HCP5 promotes colon cancer development by activating AP1G1 via PI3K/AKT pathway

Abstract

Objective: To explore whether HCP5 participates in the pathogenic progression of colon cancer (CC) and its underlying mechanism.

Patients and methods: HCP5 expression in CC tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between the HCP5 expression and tumor stage of CC patients was then analyzed. After CC cells were transfected with HCP5-siRNA, the proliferation and migration capacities were detected by cell counting kit-8 (CCK-8), colony formation and transwell assay, respectively. Cell cycle was examined by flow cytometry. Western blot was conducted to detect protein expressions of HCP5, AP1G1 and relative molecules in the PI3K/AKT pathway. Rescue experiments were performed by co-transfection of HCP5-siRNA and AP1G1-siRNA into CC cells, followed by cell function detection.

Results: HCP5 was highly expressed, whereas AP1G1 was lowly expressed in CC tissues and cell lines. Besides, CC patients with stage III-IV presented higher expression of HCP5 than those with stage I-II. The knockdown of HCP5 in CC cells down-regulated proliferation and migration capacities, and arrested cell cycle in the G0/G1 phase, which was reversed by the AP1G1 knockdown. In addition, HCP5 knockdown up-regulated AP1G1 expression, whereas down-regulated the expression of relative proteins in the PI3K/AKT pathway.

Conclusions: HCP5 was significantly increased in CC and enhanced the proliferation and migration of CC cells by inhibiting the AP1G1 expression. HCP5 promoted CC development by activating the PI3K/AKT pathway.