Cortactin Could Regulate Proliferation and Apoptosis of Esophageal Squamous Carcinoma Cells Through PI3K-AKT Pathway

Objective To investigate the effects and potential regulatory mechanisms of Cortactin (CTTN) on the proliferation and apoptosis of esophageal squamous cell carcinoma (ESCC).

Methods CTTN was overexpressed or knocked down in EC109 and TE1 cells by lentivirus infection; then Western blot was used to detect the expression of PCNA, cleaved-PARP, cleaved-Caspase3 and the key proteins of PI3K-AKT pathway; CCK-8 assay and plate colony formation assay were performed to detect cell viability and colony formation, respectively. Soft agar assay was performed to evaluate the tumorigenicity of cells in animals. Meanwhile, xenograft model of EC109 cells was used to determine the effect of CTTN knockdown on the growth of transplant subcutaneous tumor in nude mice.

Results Stable CTTN over-expression or knockdown models of EC109 and TE1 cells were successfully established. Over-expression of CTTN not only increased the expression levels of PCNA, p-PI3K and p-AKT, but also decreased the expression of cleaved Caspase-3 and cleaved-PARP, as well as improved cell activity and promoted clone formation; the effect was opposite when CTTN was knocked down (all P < 0.001).

Conclusion CTTN could promote the proliferation and inhibit the apoptosis of esophageal cancer cells through PI3K-AKT pathway.