Green tea catechins and prostate cancer: mechanisms, clinical evidence, and safety: a narrative review.

Introduction
The International Agency for Research on Cancer (IARC) estimated that approximately 20 million new cancer cases and 9.7 million cancer-related deaths occurred worldwide in 2022, with one in six of all deaths being due to cancer [1]. Prostate cancer (PCa) is the second most common cancer among men worldwide [2]. As cancer cells grow and proliferate, the functions of the prostate gland are disrupted and health problems begin to occur [3]. Although the aetiology of PCa is not clearly understood, it is a multifactorial disease, and as the risk of developing PCa increases with age, the prognosis is generally worse and the mortality rate and speed of progression also increase [2, 4]. African American men have a higher incidence of PCa and a higher mortality rate than white American men, while the lowest PCa incidence is typically found in Asian men. In addition to genetic predispositions, the disease is also associated with dietary, lifestyle, social, and environmental factors [5, 6]. Five single-nucleotide polymorphisms have been identified that are significantly associated with PCa when present in individuals with a family history of PCa [2]. They have been shown to play a role in both mitogenic and antiapoptotic events in PCa biology and PCa cell lines [7]. Studies have also found that high circulating concentrations of insulin-like growth factor-1 (IGF-1) are positively associated with both short-term and long-term PCa risk [8, 9].
Current understandings of the relationship between adiposity and tumour development are based on the assumption that adiposity involves changes in metabolism and endogenous hormone levels [10]. Thus, a positive relationship has been described between obesity and PCa [11]. It is thought that functional polymorphisms in genes involved in polycyclic aromatic hydrocarbon metabolism and detoxification may alter smoking’s effects on PCa, and a higher recurrence rate was reported for patients who smoked during treatment compared to lifelong nonsmokers and for those who smoked before but quit compared to lifelong nonsmokers [12–14].Excessive consumption of alcohol is also known to be a possible risk factor for all types of cancer, including PCa [15].
PCa is an age-related disease and the prognosis of high-grade PCa is typically poor. Surgical treatment of the disease may also negatively affect patients’ quality of life [4]. In recent years, polyphenolic compounds, together with macro- and micronutrients, have attracted attention for their possible relationships with and effects on many diseases, particularly cancer. Among the many compounds being investigated for both chemopreventive and therapeutic effects against PCa, green tea polyphenols (GTPs) seem to be especially promising [16]. During green tea (GT) production, the endogenous oxidase enzymes in the tea leaves are inactivated by heating, thus preserving the GTPs in comparison to other types of tea. These catechins include epigallocatechin gallate (EGCG), epigallocatechin (EGC), epicatechin gallate (ECG), epicatechin (EC), gallocatechin (GC), and catechin (C) [17]. EGCG accounts for more than half of the total catechin content in GT leaves. While it has been stated that the EGCG found in GT may constrain the occurrence and progression of PCa by inhibiting cell proliferation, inducing apoptosis, preventing invasion and metastasis, and modulating various other pathways, there are inconsistencies in the literature among the results obtained in clinical studies [18, 19]. Studies have indicated that EGCG may prevent carcinogenesis by exhibiting MMP and anti-angiogenic properties, inhibiting key signalling pathways, and activating redox-sensitive transcription factors [20, 21]. However, the development of effective EGCG-based therapeutic strategies requires further refinement in terms of stability, specificity, absorption, bioavailability, and reliability [22].
In this narrative review, we synthesize the mechanisms by which green tea catechins (GTCs), particularly EGCG, may influence the carcinogenesis and progression of PCa, and we summarize the clinical evidence stratified by formulation, dose, and duration, including safety, while identifying gaps and priorities for future trials.

Methods
This study aims to clarify the relationships between EGCG and PCa. A literature search was conducted using the Web of Science, PubMed, Google Scholar, ScienceDirect, and Scopus databases. The following keywords were used during the search: “green tea”, “tea”, “Camellia sinensis”, “polyphenols”, “catechins”, “green tea catechins”, “epigallocatechin gallate”, “prostate cancer”, “signalling pathway”, “IGF-1, “NF-κB”, “MAPK”, “JAK/STAT”, “Wnt/β-catenin”, “PI3K/Akt/mTOR”, “AMPK”, “‘TGF-β/SMAD”, “COX-2”, “cell cycle”, “apoptosis”, “anticancer”, “molecular mechanisms”, “cellular mechanisms”, “obesity”, and “risk factors”.
Only full-text articles published in English were included. Eligible study types included original research articles, reviews, systematic reviews, meta-analyses, compilations, and letters to the editor. Studies published as non-peer-reviewed preprints or written in languages other than English were excluded. Articles not directly related to the predefined research themes, as determined by titles and abstracts, were also excluded. The final selection included 102 studies published primarily between 2016 and 2025.

Nutritional composition of Green Tea (GT)
GT is obtained from the Camellia sinensis plant, and particularly from the Camellia sinensis var. assamica variety, which is known for its high polyphenol contents. This elevated concentration of polyphenols contributes to the strong bitterness often associated with GT [23]. GT has a complex composition including a variety of beneficial bioactive and nutritional compounds. It possesses proteins and a variety of amino acids such as theanine (or 5-N-ethyl-glutamine), glutamic acid, tryptophan, glycine, serine, aspartic acid, tyrosine, valine, leucine, threonine, arginine, and lysine. The carbohydrates present in GT include cellulose, pectin, glucose, fructose, and sucrose [24–27].
The lipid profile of GT features linoleic and α-linolenic acids, along with plant sterols such as stigmasterol. GT also contains essential vitamins, xanthine derivatives including caffeine and theophylline, and various pigments such as chlorophyll and carotenoids. Additionally, GT is rich in volatile compounds such as aldehydes, alcohols, esters, lactones, and hydrocarbons, which contribute to its aroma and flavour [24, 26]. Mineral and trace elements include potassium, magnesium, iron, zinc, calcium, copper, selenium, sodium, phosphorus, and fluoride [24–27]. Flavonoids are an important class of phenolic compounds widely distributed in plants, present in considerable amounts ranging from 0.5% to 1.5% and comprising over 4,000 identified varieties [26]. The primary flavonoids present in GT belong to the catechin group (flavan-3-ols), including the four major catechins of EGCG, EGC, ECG, and EC. EGCG is the most abundant catechin, constituting approximately 60% of the total catechins in GT, followed respectively by EGC (19%), ECG (13.6%), and EC (6.4%) [27, 28]. In addition to these catechins, GT contains gallic acid and other phenolic acids such as chlorogenic and caffeic acids, as well as flavonols including kaempferol, myricetin, and quercetin [24, 27, 28]. Tea leaves are also rich in hydrolysable tannins, including ellagitannins and gallotannins, which are phenolic acid derivatives noted for their antioxidant properties and potential anticancer effects [24–29].
The chemical structures of gallic acid and the four major catechins found in GT are illustrated in Fig. 1.

In addition to its antioxidant properties, EGCG exerts significant anti-inflammatory effects, including cytokine modulation, inhibition of the NF-κB signalling pathway, immune system regulation, and enhancement of vascular function. These biological activities contribute to its health-promoting potential, particularly in the prevention and management of cancer, cardiovascular diseases, gastrointestinal disorders, and liver damage. EGCG exerts these effects through multiple mechanisms, such as reducing DNA damage and oxidative stress, neutralising free radicals, detoxifying carcinogens, and modulating the expression of genes associated with carcinogenesis [22, 30].

Potential effects of Green Tea Catechins (GTCs) on Prostate Cancer (PCa)
The anticancer properties of GTCs in terms of both prevention and treatment have been reported in various studies as being effective against both PCa, as a cancer type involving solid tumours, and against other types of solid-tumour cancers [31, 32]. Most of the anticancer effects of GT are mediated by these catechins. Among them, EGCG has the most pronounced impact and the strongest inhibitory power, respectively followed by ECG, EGC, and EC. GT was found to have better antitumour activity than pure EGCG due to the synergistic effect of its combined catechins. However, it was also reported that EGCG protects against cancer by increasing apoptosis and cell cycle arrest, reducing the proliferation of cancer cells, reducing angiogenesis, and exerting various anti- and pro-oxidant effects [32]. It has also been reported to support cancer treatment by amplifying the anticancer effects of chemotherapy and radiotherapy, increasing the drug concentrations in plasma and other cells, impacting hormone receptor-related signalling pathways and chemoresistance- and radioresistance-related molecular pathways, affecting redox-regulated processes, making the body more sensitive to chemotherapy and radiotherapy, and reducing oxidative damage and inflammation to ameliorate the negative effects that occur during cancer treatment [30, 32, 33].
The diverse ways in which ECCG may exert its effects in preventing cancer and supporting cancer treatment are shown in Fig. 2.

EGCG can block the protein kinases linked to cell growth and activate the protein kinases associated with cell apoptosis; furthermore, it suppresses proteinases such as MMPs, inhibiting the migration, invasion, and metastasis of cancer cells. It has also been confirmed that EGCG exhibits antioxidant, anti-inflammatory, antiproliferative, antiangiogenic, and antimetastatic properties at different stages of tumour development by modulating signalling pathways, enzymatic functions, and protein kinases [30, 32].

Some pathways through which Green Tea Catechins (GTCs) May play roles in Prostate Cancer (PCa)
The nuclear factor kappa B (NF-κB) signalling pathway plays a crucial role in regulating a wide array of biological responses that contribute to malignant progression in various cancers, including PCa. Overactivation of the NF-κB pathway has been implicated in the development of primary PCa as well as the progression to metastatic castration-resistant PCa [34]. Catechins increase tumour necrosis factor-alpha (TNF-α) levels, which in turn suppresses NF-κB activity and thus induces apoptosis [35]. The EGCG-induced inactivation of NF-κB is associated with the phosphorylation-dependent degradation of the IκB inhibitor, leading to increased nuclear translocation of the p65 subunit and inhibition of IκB kinase activity. NF-κB and its associated components are widely recognised for their critical roles in PCa progression through the regulation of tumour growth, apoptosis, angiogenesis, and metastasis [36, 37]. The interplay between NF-κB and other signalling molecules, such as androgen receptor (AR), IGF and the IGF receptor axis, and cyclooxygenase-2 (COX-2), is crucial in PCa progression [36]. Catechins also increase nuclear factor erythroid 2-related factor 2 (Nrf2) expression by inhibiting the NF-κB pathway [38]. This inhibition downregulates the antiapoptotic Bcl-XL gene, promoting apoptosis and contributing to the anticancer effects of catechins [39]. Dysregulation of NF-κB accelerates carcinogenesis by enhancing cell proliferation, invasion, and resistance to therapy. Upregulation of NF-κB is observed during PCa progression, leading to faster cell cycle advancement and increased proliferation rates [40]. Moreover, NF-κB overexpression contributes to chemotherapy and radiotherapy resistance, whereas its inhibition via antitumor agents can potentially slow cancer progression. Noncoding RNAs have been reported to modulate NF-κB expression and nuclear translocation, offering a potential therapeutic strategy to control PCa progression [40, 41].
Furthermore, EGCG interacts with peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1), mediating its inhibitory effect on the NF-κB signalling pathway in PCa. This interaction alters transcriptional regulation, enhances the onco-suppressive properties of EGCG, and affects cancer cell proliferation and survival [42].
Mitogen-activated protein kinases (MAPKs) constitute a family of serine/threonine-specific, proline-directed protein kinases that play essential roles in regulating signal transduction pathways. These kinases are evolutionarily highly conserved and are present in all eukaryotic cells, where they regulate diverse cellular processes [43]. The MAPK family includes several subgroups, such as extracellular signal-regulated kinases 1 and 2 (ERK1/2), p38 MAPK, and c-Jun N-terminal kinases 1, 2, and 3 (JNK1/2/3, also known as stress-activated protein kinase), as well as ERK3/4, ERK5, and ERK7/8 [44, 45].
Signalling cascades initiated by membrane-bound receptor tyrosine kinases regulate both the cell cycle and the initiation of programmed cell death. Within these cascades, Ras activates Raf-1, which subsequently phosphorylates and activates ERK1/2. The effects of EGCG and theaflavins on the phosphoinositide 3-kinase/protein kinase B (PI3K/PKB) and MAPK pathways have been investigated. Treatment with both EGCG and theaflavins was shown to decrease PI3K and phosphorylated Akt levels while increasing ERK1/2 activation in the DU145 and LNCaP PCa cell lines, suggesting that ERK1/2 may contribute to the anticancer properties of these compounds [44, 45].
EGCG has also been demonstrated to inhibit the activation of MMP-2 and MMP-9 in DU145 cells, an effect potentially mediated through the suppression of ERK1/2 and p38 MAPK phosphorylation, both of which are critical for MMP activation. This reduction in MMP activity implies a possible role of EGCG in inhibiting tumour invasion and metastasis [46, 47]. Furthermore, the MAPK pathway has been reported to be downregulated in response to EGCG treatment, likely due to the decreased phosphorylation of ERK1/2 and the inhibition of upstream Raf-1 and Ras activities [48, 49].
The Janus kinase and signal transducers and activators of transcription (JAK/STAT) signalling pathway plays a pivotal role in intercellular communication, governing various physiological and pathological mechanisms. Growing interest in the intricate connection between the dysregulation of this pathway and the advancement of malignant tumours is arising. Therapeutic compounds targeting the JAK/STAT signalling pathway, including plant-derived compounds, synthetic medications, and biomolecules, may exhibit anticancer properties through multiple mechanisms, such as inhibiting cell proliferation, triggering programmed cell death, and suppressing the spread of tumours and blood vessel formation [50]. Since STAT proteins are transcription factors, their basic regulatory mechanism is based on the control of gene transcription. In addition to acting as transcription factors, STAT proteins have been reported to regulate different signalling pathways that are effective in PCa survival and progression, and the NF-κB of activated B cells is usually continuously active in PCa [47, 51, 52]. EGCG is a compound capable of inhibiting the JAK/STAT signalling pathway and can prevent cell proliferation and tumour development by suppressing the phosphorylation of JAK kinases and STAT proteins [47]. Catechin blocks tumour angiogenesis by inhibiting EGFR, which in turn reduces the expression of various proteins including ERK1/2, AP1, VEGF, PKB, and IL-8, ultimately halting the process of angiogenesis. Additionally, catechin enhances the antitumor immune response by modulating the JAK/STAT signalling pathway, specifically by inhibiting the phosphorylation of STAT3.36 In PCa cells, EGCG has been found to inhibit STAT3 activity, halting the growth of cancer cells and increasing apoptosis. This mechanism could explain the therapeutic potential of EGCG against PCa [52]. It is known that the JAK/STAT pathway plays an important role in the progression of metastasis. EGCG can prevent metastasis by inhibiting this pathway, and it has also been shown that EGCG reduces the motility and invasion of PCa cells with metastatic properties [53]. The JAK/STAT pathway affects the immune response by regulating the function of immune cells and inflammation around the tumour. By modulating this pathway, EGCG may encourage immune cells to respond more effectively to the tumour and slow down the evolution of the cancer [52, 53].
The PI3K/Akt/mTOR signalling pathway is a classic apoptotic regulatory pathway that can regulate multiple apoptosis-related proteins or families [54]. Abnormal activation of this pathway can trigger excessive proliferation and differentiation of tumour cells, inhibit cell apoptosis, increase cell tolerance to hypoxia and nutrient depletion, and promote the metastasis of tumour cells. Catechin causes cell cycle arrest by inhibiting the PI3K/AKT pathway and decreases proliferation by reducing cyclin D1 and blocking mTOR [35]. Therefore, EGCG exerts important biological effects by inhibiting the PI3K/Akt/mTOR pathway in PCa cells. Studies have found that EGCG inhibits cell growth and increases apoptosis by suppressing the activity of this pathway in Du145 PCa cells [55].
The Wnt/β-catenin signalling pathway consists of proteins that play important roles in embryonic development and tissue homeostasis. The relevant gene is active in various cellular processes including cell growth, migration, programmed cell death, and differentiation, while also regulating several other genes. Disruptions in Wnt/β-catenin signalling can lead to many serious diseases, including both cancers and other non-cancerous diseases [56]. It has been shown that Wnt/β-catenin may play roles in pathogenesis, metastasis, and resistance to treatment in PCa, as well as many other types of cancer [57]. It regulates the Wnt signalling pathway by breaking down β-catenin, preventing the transcription of MMPs, and restricting tumour cell migration [35]. Circulating tumour cells (CTCs) play a major role in the current understanding of the metastatic potential of cancer. Studies of PCa and pancreatic cancer have found that CTCs are associated with Wnt signalling, and this signalling increases the metastatic capacity of cancer cells [58]. In addition, the noncanonical Wnt signalling pathway is active in prostate CTCs resistant to androgen receptor suppression [59], indicating that Wnt signalling may promote metastasis and angiogenesis. EGCG inhibits the transportation of β-catenin to the nucleus by inhibiting the Wnt/β-catenin pathway, reduces its transcriptional activities, and decreases β-catenin levels by increasing GSK3β expression; these effects of EGCG suggest that it could potentially be used as a therapeutic tool in cancer treatment [60].
The AMP-activated protein kinase (AMPK) signalling pathway is based on AMPK, a heterotrimeric complex consisting of three subunits that control cellular metabolism, increase insulin sensitivity, and regulate cell growth [61]. In one study, the genetic and pharmacological activation of AMPK was found to have a protective effect on PCa progression and to increase PGC1α expression, leading to catabolic metabolic changes; this was marked by elevated mitochondrial gene expression, enhanced fatty acid oxidation, reduced cell proliferation, and diminished cell invasiveness, thus preventing PCa progression [62]. In another study, EGCG was found to significantly increase AMPK activity and increase the rate of proapoptotic events. EGCG triggers AMPK activation, resulting in metabolic reprogramming, which can inhibit cellular growth, proliferation, and invasion [63]. Activation of MPK leads to changes such as increased energy production and promotion of fatty acid oxidation. This mechanism supports the potential of EGCG in cancer treatment [64].
The transforming growth factor-beta/Sma- and Mad-related protein (TGF-β/SMAD) signalling pathway is based on TGF-β, a secreted cytokine family that includes the three isoforms of TGF-β1, TGF-β2, and TGF-β3 [65]. TGF-β1 plays a significant role in oncological malignancy and the development of the tumour microenvironment [66]. The relationship between PCa and TGF-β is complex because TGF-β signalling has both onco-suppressive and oncogenic functions. Nevertheless, the majority of studies conducted to date strongly support the role of TGF-β signalling in enhancing the migration of PCa cells [67]. TGF-β signalling can promote metastasis by promoting the migration of PCa cells, but it also promotes cancer progression by inhibiting the antitumor response of immune cells [68]. Therefore, the blocking of TGF-β signalling may offer a viable strategy for the treatment of PCa, similarly to other types of cancer [67, 69]. EGCG has been shown to suppress invasive phenotypes triggered by TGF-β1, invasive and migratory activities, MMP-2 secretion, and cell adhesion [70]. One study revealed that EGCG blocks the expression of genes related to TGF-β-induced epithelial-mesenchymal transitions by inhibiting the formation of reactive oxygen species (ROS), SMAD phosphorylation, and nuclear translocation [71]. Although no study has been conducted directly on EGCG’s role in PCa via TGF-β, the effectiveness of TGF-β in PCa and the inhibitory effects of EGCG on TGF-β in studies conducted on other cancers indicate that EGCG may have potential preventive and/or therapeutic effects against PCa and that more research is required.
The IGF-1 signalling pathway also plays a significant role in the development and progression of PCa. IGF-1, together with other members of the IGF family, is involved in cellular growth, proliferation, and survival processes critical to cancer development. As a potent mitogen, IGF-1 has been associated with an increased risk of PCa. IGFs also influence various aspects of carbohydrate, lipid, and protein metabolism while playing key roles in regulating cell growth, differentiation, apoptosis, and transformation [72]. Notably, only the free form of IGF-1 can bind to the specific receptor IGF-IR, thereby inducing cell proliferation and differentiation and preventing apoptosis. IGF-1 is recognised as a key growth factor in the onset of cancers across multiple organs [72, 73].
Upon the binding of IGF ligands to their receptors, autophosphorylation occurs within the receptor, leading to the phosphorylation of various cellular substrates. This activation triggers several downstream signalling pathways, including the PI3K/Akt and Ras/MAPK pathways, which stimulate gene expression, DNA replication, and cell division [72, 74]. In the context of PCa, EGCG has been shown to inhibit IGF-1 signalling, as evidenced by decreased IGF-1 receptor phosphorylation, and to reduce downstream Akt activation, thereby impeding cancer cell survival and metastasis. Furthermore, EGCG enhances apoptosis in PCa cells, thereby contributing to its chemopreventive effects [24].
Additionally, an in vivo study demonstrated that mice orally administered GTPs exhibited decreased serum IGF-1 levels and increased insulin-like growth factor binding protein 3 (IGFBP-3) levels compared to controls receiving water [35]. While EGCG thus shows promise in inhibiting IGF-1 signalling, the complexity of cancer biology suggests that multiple pathways may contribute to PCa progression, indicating that a multifaceted therapeutic approach may be necessary for effective prevention and treatment [74]. Human studies are essential to establish a clear and meaningful relationship between the IGF-1 signalling pathway and EGCG in PCa research.
The cyclooxygenase (COX)−2 signalling pathway is based on COX, a key rate-limiting enzyme in the biosynthesis of prostaglandins. It is found in two isoforms, COX-1 and COX-2. COX-2, a regulated enzyme, plays a significant role in inflammation and pain, being upregulated by mitogens, oncogenic agents, cytokines, and proliferation-inducing molecules across various cell types; its expression is regulated at both transcriptional and post-translational levels [75], and its overexpression has also been associated with cancer progression [76]. COX enzymes have been found to play an important role in PCa progression and prognosis. In particular, the level of COX-2 is increased in PCa cells, and this increase may be associated with tumour growth [77]. EGCG inhibits the relocation and occupation of cancer cells by specifically targeting COX-2. It also triggers programmed cell death in malignant cells and reduces the levels of inflammation-associated molecules, and EGCG modulation of COX-2 gene expression offers a potential mechanism of action in the therapy and prevention of cancer [78].
Some pathways by which GT catechins, and especially EGCG, may play a role in PCa are given in Fig. 3, while EGCG’s mechanisms of effect in PCa and the relevant affected pathways are given in Table 1.

The effect of epigallocatechin gallate on cell cycle regulation is also important as cell cycle dysregulation is one of the basic markers of cancer. Many studies have identified a link between cell cycle control and cancer [79]. The exposure of PCa LNCaP and DU145 cells to EGCG revealed that WAF1/p21, KIP1/p27, INK4a/p16, and INK4c/p18 protein expression levels increased; cyclin D1, cyclin E, and cdks-2, −4, and − 6 protein expression levels decreased; cyclin D1 binding to WAF1/p21 and KIP1/p27 increased; and cyclin E binding to cdk2 decreased [80]. Studies have shown that EGCG arrests the cell cycle in the G1 phase, inhibits proliferation, and promotes apoptosis. This effect is mediated by cyclin-dependent kinase inhibitors (p21 and p27) and cell cycle regulators such as cyclin D1. In addition, EGCG has been reported to inhibit the growth of PCa cells by suppressing androgen receptor signalling. These results indicate that EGCG has potential as an adjuvant agent in the treatment of PCa [79, 80].

Recent studies on Green Tea (GT) catechins and Prostate Cancer (PCa)
In one clinical study, tea polyphenols were found in the prostate tissue of the participants who consumed GT, and notable declines in NF-κB expression and prostate-specific antigen (PSA) levels were also observed. The antioxidant effect and the decrease in serum PSA levels were found only in the group that consumed GT. It was suggested that EGCG and other catechins might be beneficial in decreasing inflammation and DNA damage [81]. In a phase II, randomised, placebo-controlled study [82], EGCG levels were found to be higher in the group receiving EGCG capsules compared to the placebo group, but the highest levels were observed in the group that consumed three cups of GT daily for 6 months among men at high risk of PCa. Although EGCG appeared to have the potential to reduce the risk of PCa, no significant difference was observed in individuals’ PSA levels. In the prospective randomised study conducted by Henning et al. [33], GTPs had significantly higher concentrations in the blood and prostate tissue of PCa patients who consumed four cups of GT per day, indicating that these compounds may provide potential therapeutic benefits in the treatment of PCa. It was also shown that GT catechins, and especially EGCG, modulate molecular pathways in prostate carcinogenesis, may aid in chemoprevention, and could help to improve clinical decision-making in treatment strategies, especially for low-grade PCa managed through active surveillance [83]. In the study conducted by Yeo et al. [84], it was determined that EGCG suppressed the formation of vasculogenic mimicry in PCa cells by inhibiting the twist/VE-cadherin/AKT signalling pathway and that EGCG could be used as a potential therapeutic agent in the treatment of PCa with the possibility of reducing cancer progression by inhibiting the ability of cancer cells to form vascular-like structures. Deb et al. [85] also showed that GT inhibited HDACs and other epigenetic enzymes in PCa development, induced the re-expression of TIMP-3, and prevented the invasion and metastasis of PCa cells. Thus, they determined that GT may be a potential therapeutic option in the treatment of PCa due to its effects on epigenetic modulation [85].
Another study emphasised that GT consumption may decrease the occurrence of PCa in a dose-dependent manner, with intake of more than 7 cups/day considerably reducing the risk of PCa. It was further stated that the EGCG found in GT might provide a safeguard against PCa by inhibiting angiogenesis, metastasis, and cell growth and inducing apoptosis. However, inconsistencies in the sizes of the cups, the amounts of GT in the cups, and brewing processes were reported to be limitations of the study preventing generalisation [18].
EGCG has been reported to inhibit PCa progression by reducing serum IGF-1 and PSA levels, inducing cell cycle arrest, and promoting apoptosis; furthermore, it has been shown to act as a radiosensitiser in radiotherapy, demonstrating significant therapeutic potential against PCa [86]. GT catechins considerably diminished the risk of PCa in one study, suggesting that they may play a beneficial role in PCa prevention compared to other dietary antioxidants [87]. Another study indicated that catechins from GT can alter the levels of various relevant biomarkers involved in prostate carcinogenesis and the clinical progression of PCa without major side effects. That study concluded that GT can play an effective role in the prevention and treatment of PCa, and other prostate conditions as well, through the modulation of NF-κB and systemic oxidation, but more studies are needed to make definitive recommendations [31]. Mokhtari et al. [88] showed that EGCG increased the antitumor effect of miR-34a and inhibited cell proliferation and metastasis by suppressing the oncogenic effect of miR-93. In another study, the effectiveness of EGCG itself and that of an EGCG nanoformulation in a 3D spheroid model of PCa were compared. In this study, the free form and the nanoformulation of EGCG were evaluated in terms of cell proliferation, apoptosis, and metastasis markers, and the results showed that nanoformulated EGCG had higher bioavailability, suppressed tumour growth more significantly, and increased apoptosis [89]. Alserihi et al. [90] reported that EGCG suppressed tumour growth and induced apoptosis by increasing cellular uptake, concluding that nanoparticle forms of EGCG may facilitate more effective treatment strategies. Devi et al. [91] showed that GT catechins, and especially EGCG, suppressed cancer cell proliferation and prevented metastasis by changing the tumour microenvironment. Guo et al. [92] also showed that nanovesicles containing tea polyphenols strengthened the immune response, suppressed tumour growth, and may be an effective strategy in treating PCa. Another study demonstrated that catechins, and especially EGCG, exerted inhibitory effects against tumour formation by increasing apoptosis, suppressing cell proliferation, and inhibiting angiogenesis in various cancers, including PCa [93].
A review study concluded that EGCG possesses antioxidant, anti-inflammatory, and anticarcinogenic properties and highlighted the existence of an inverse correlation between GT consumption and the risk of PCa, suggesting that GT may offer protective benefits against more aggressive forms of the disease. Additionally, various components of GT were shown to promote apoptosis and influence key signalling pathways involved in the progression and development of PCa, and GT consumption was associated with a decrease in PSA and tumour marker levels, playing a potential role in slowing the progression of the disease [94]. GT, as an unfermented tea, has rich polyphenol contents and EGCG is one of its most beneficial bioactive compounds, being the main phytocompound responsible for the various pharmacological effects of GT, and especially its antioxidant effects [95]. One study reported that EGCG suppressed cancer progression in both androgen-independent (DU-145 and PC-3) and androgen-sensitive (LNCaP and CWR22Rv1) PCa cell lines in a dose-responsive fashion, and the toxicity of GT was reported for PCa cells. Toxicity was mediated by oxidative stress triggered by Akt downregulation, and a relationship was suggested between the antiproliferative and pro-oxidant effects of polyphenol E in PC-3 cells [24]. Polyphenol E modulated molecular signalling to exert toxicity in PC-3 cell lines [96].
Thus, studies have shown the promising anticancer effects of GT catechins against various cancers, including PCa, which are exerted by regulating ROS and targeting cancer stem cells. These findings emphasise the potential of these catechins as effective antioxidants and anticancer agents [97].

Safe levels and toxic effects
The European Food Safety Authority (EFSA) has assessed the safety of dietary GT catechins, considering the potential for adverse effects on the liver. Those analyses showed that catechins from GT infusions and other similar beverages are generally safe. When taken as a dietary supplement, catechins at daily doses of 800 mg or more may pose a health risk, but most relevant studies have focused on supplements containing 200–800 mg of EGCG or individuals consuming 3–5 cups of GT per day [98]. One cup of GT (250 mL of hot water and 2.5 g of tea leaves) contains 96 mg of EGCG; thus, consuming 3 cups of GT per day is sufficient to achieve the full effect of these catechins, allowing for daily consumption levels of 200–300 mg [99]. Some animal and human studies have reported toxic effects alongside the health benefits of GT, but the doses applied in these studies and the effects of those doses have varied. The EFSA concluded that generalising about a single dose that can be considered safe for GT is not possible [98]. The wide range of doses that may trigger toxic effects suggests that genetic predispositions and liver health may also affect toxicity levels.
More studies are needed to shed light on these issues [100]. To achieve the health benefits of GT, it is important to consume it in appropriate amounts together with dietary supplements that will increase its bioavailability. Furthermore, GT should not be consumed on an empty stomach; it should be taken with meals, and it should not be consumed by individuals with liver disorders. Excessive consumption can have negative effects on the liver. GT can interact with blood-thinning drugs, especially warfarin. It can reduce iron absorption; thus, individuals with iron deficiency should be careful about their GT consumption levels.
Regular consumption of GT or controlled EGCG supplementation may support prostate health. However, it is important to consult a doctor before using any supplements.

Limitations
The primary goals of cancer prevention and treatment are to prevent DNA damage, angiogenesis, and metastasis while promoting apoptosis. Studies conducted with cell lines and experimental animals have enhanced our understanding of the molecular effects of EGCG on cancer cells. However, most of this research has been based on in vivo and in vitro studies with cell cultures and animal models. EGCG has been shown to inhibit angiogenesis, migration, proliferation, metastasis, and tumour growth in PCa cells, as well as to induce apoptosis. Our synthesis is narrative and may have missed studies not indexed in English; we did not apply standardized risk-of-bias tools. Variability in formulation, dose, and duration and the lack of pharmacokinetic measures in many trials limit comparability and may explain contradictory findings. Most clinical outcomes derive from small studies. Further clinical, experimental, and epidemiological studies are needed to determine the optimal dosage of EGCG, its stage-specific effects, brewing methods and durations when it is consumed in GT, duration of use, potential side effects, dose-response relationships, and drug interactions. Moreover, individual cases should be evaluated holistically, considering genetic backgrounds, physical and social environments, and lifestyles.

Conclusion and recommendations
Despite promising preclinical and clinical evidence suggesting potential chemopreventive effects of GTCs, particularly EGCG, on PCa, current data remain insufficient to support their clinical application for prevention or treatment. Most available studies are limited by small sample sizes, short intervention durations, inconsistent endpoints, and dosing regimens. These methodological inconsistencies hinder the comparability of findings and the establishment of evidence-based recommendations. To address these gaps, future research should focus on rigorously designed, placebo-controlled randomized trials employing standardized GT extracts or purified EGCG preparations within a defined dosage range (200–800 mg/day), conducted in well-characterized high-risk populations such as men with elevated PSA levels or premalignant lesions. Long-term studies integrating molecular and clinical outcomes are warranted to elucidate dose-response relationships, safety profiles, and underlying mechanisms of action. In conclusion, the true chemoprotective potential of GTCs in PCa can only be established through such standardized and comprehensive investigations. Given the increasing global incidence of PCa, the need for these studies is urgent.

Future perspectives
More detailed molecular investigations are needed to identify the specific biochemical pathways targeted by GTCs in PCa, as well as the genes and proteins they regulate. Clinical studies exploring different dosage levels are needed to optimise the therapeutic efficacy of GTCs while minimising toxicity. In particular, determining the ideal concentrations of active compounds such as EGCG is critical. Exploring the effects of GTCs in combination with existing therapeutic modalities including hormone therapy and immunotherapy could enhance treatment outcomes and support personalised medicine strategies. Nanotechnology-based delivery systems are promising for enhancing the anticancer efficacy of EGCG by improving its bioavailability and prolonging its systemic activity. The clinical evaluation of such nanoformulations constitutes a vital direction for future research. Additionally, large-scale epidemiological studies are needed to assess the association between GT consumption and PCa incidence across various age groups. These studies could provide valuable insight into the long-term chemopreventive properties of catechins and the influence of dietary habits on cancer risk. It is also essential to examine how genetic predispositions and environmental factors modulate these relationships.

Supplementary Information