Investigating the material basis and molecular mechanisms of in the treatment of papillary thyroid carcinoma: a network pharmacology and experimental study.
[BACKGROUND] Papillary thyroid carcinoma (PTC) is among the most prevalent forms of thyroid cancer.
APA
Ding C, Shi TF, et al. (2026). Investigating the material basis and molecular mechanisms of in the treatment of papillary thyroid carcinoma: a network pharmacology and experimental study.. Translational cancer research, 15(2), 106. https://doi.org/10.21037/tcr-2024-2675
MLA
Ding C, et al.. "Investigating the material basis and molecular mechanisms of in the treatment of papillary thyroid carcinoma: a network pharmacology and experimental study.." Translational cancer research, vol. 15, no. 2, 2026, pp. 106.
PMID
41822120
Abstract
[BACKGROUND] Papillary thyroid carcinoma (PTC) is among the most prevalent forms of thyroid cancer. Traditional Chinese medicine (TCM) has been widely employed in the management of PTC, with (OD) demonstrating potential in cancer treatment. This study aimed to investigate the anti-PTC effects of OD and elucidate the underlying mechanisms.
[METHODS] The impact of OD on PTC cells was assessed using a variety of assays, including cell viability, colony formation, acridine orange/ethidium bromide (AO/EB) staining, and transwell assays. Potential targets and downstream pathways were explored through network pharmacology and molecular docking analyses. Protein and gene expression levels were determined using western blotting assays.
[RESULTS] OD demonstrated significant inhibitory effects on the biological functions of PTC cells. Through network analysis, 7 targets and 3 active compounds (stigmasterol, β-sitosterol, or poriferasterol) associated with OD's intervention in PTC were identified. Furthermore, correlation analysis revealed a significant positive association with the central gene involved in OD's anti-PTC effects. OD and its active compounds also modulated the phosphorylation of proteins related to the PI3K-AKT pathways, underscoring its anti-PTC efficacy.
[CONCLUSIONS] OD and its active compounds suppress the biological functions of PTC by modulating the phosphorylation of proteins associated with the PI3K-AKT pathway. These findings suggest that OD may inhibit PTC progression by targeting the PI3K-AKT pathway, offering potential adjuvant therapeutic value for PTC.
[METHODS] The impact of OD on PTC cells was assessed using a variety of assays, including cell viability, colony formation, acridine orange/ethidium bromide (AO/EB) staining, and transwell assays. Potential targets and downstream pathways were explored through network pharmacology and molecular docking analyses. Protein and gene expression levels were determined using western blotting assays.
[RESULTS] OD demonstrated significant inhibitory effects on the biological functions of PTC cells. Through network analysis, 7 targets and 3 active compounds (stigmasterol, β-sitosterol, or poriferasterol) associated with OD's intervention in PTC were identified. Furthermore, correlation analysis revealed a significant positive association with the central gene involved in OD's anti-PTC effects. OD and its active compounds also modulated the phosphorylation of proteins related to the PI3K-AKT pathways, underscoring its anti-PTC efficacy.
[CONCLUSIONS] OD and its active compounds suppress the biological functions of PTC by modulating the phosphorylation of proteins associated with the PI3K-AKT pathway. These findings suggest that OD may inhibit PTC progression by targeting the PI3K-AKT pathway, offering potential adjuvant therapeutic value for PTC.
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