The feasible role of soluble E‑cadherin in spheroidogenesis of HCT116 colorectal cancer cells, a candidate biomarker for liquid biopsy
This study explores the role of soluble E-cadherin in colorectal cancer, particularly in the context of spheroidogenesis and malignant transformation. Although E-cadherin is widely recognized as a tumor suppressor due to its role in cell-cell adhesion, its involvement in malignant transformation remains incompletely understood.
To investigate its effects, E-cadherin knockout (KO) was induced in HCT116 colorectal cancer cells by targeting exon 3 of the CDH1 gene. Cell viability assays demonstrated that both wild-type and CDH1 KO cells exhibited similar responses to treatment with 5-fluorouracil, epidermal growth factor receptor inhibitors, and Src kinase inhibitors. Exogenous E-cadherin and the anti-E-cadherin antibody DECMA-1 did not significantly impact spheroidogenesis, though long-term maintenance of spheroids was slightly impaired in CDH1 KO cells.
Interestingly, E-cadherin expression was elevated in spheroid cultures compared to conventional monolayer cultures, with soluble E-cadherin increasing over time, particularly in wild-type HCT116 cells. The MEK inhibitor PD98059 enhanced E-cadherin expression while inhibiting ERK activation in conventional cultures, yet it did not affect spheroid formation.
These findings suggest that soluble E-cadherin could serve as a potential biomarker for colorectal cancer progression. However, GDC-0994 exogenous E-cadherin appears to have limited influence on malignant transformation, indicating that further studies are necessary to elucidate its precise mechanistic role. Would you like to explore related studies on E-cadherin’s role in tumor progression or potential therapeutic implications?