Upregulation of LTF promotes left-sided colorectal cancer development via activating PI3K/AKT pathway.

Lactoferrin (LTF) has gained attention as a potential anti-cancer biomarker, but its role in left-sided colon cancer (LCC) remains poorly understood. This study explores the function of LTF in LCC and its underlying mechanisms. LTF expression was significantly elevated in tumor tissues compared to normal tissues (59.67-fold increase,  < .001). LTF overexpression significantly enhanced LCC cell proliferation, migration, and invasion ( < .01), while suppressing apoptosis ( < .05). In contrast, LTF knockdown markedly inhibited these oncogenic behaviors. Western blot analysis demonstrated that LTF overexpression led to increased phosphorylation of PI3K and Akt proteins ( < .01), suggesting activation of the PI3K/AKT signaling pathway, while LTF knockdown resulted in decreased phosphorylation levels ( < .01). This study identifies LTF as a promoter of LCC development via activation of the PI3K/AKT pathway, suggesting LTF as a promising therapeutic target. Further research is warranted to evaluate its clinical potential in LCC treatment.