GINS2 regulates the proliferation and apoptosis of colon cancer cells through PTP4A1.

Colon cancer is associated with high death rates worldwide and poses a serious threat to public health. GINS complex subunit 2 (GINS2) serves a carcinogenic role in many cancers, including gastric adenocarcinoma, ovarian cancer and pancreatic cancer. However, the specific function of GINS2 in the development of colon cancer has not been described in detail. The present study aimed to clarify the role of GINS2 in colon cancer. A Cell Counting Kit‑8 assay, EdU staining, TUNEL and flow cytometry analyses were performed to determine the levels of cell viability, proliferation and apoptosis and to evaluate the cell cycle. Through the analysis of BioGrid, a Protein‑Protein Interaction database, it was hypothesized that protein tyrosine phosphatase 4A1 (PTP4A1) is a protein that might interact with GINS2, which was then validated using a co‑immunoprecipitation assay. mRNA and protein levels were measured using reverse transcription‑quantitative PCR and western blotting, respectively. The results of the present study demonstrated that GINS2 expression levels were increased in colon cancer cells. Furthermore, GINS2 knockdown inhibited the proliferation of colon cancer cells, while the levels of cell cycle arrest and apoptosis were increased. By interacting with PTP4A1, GINS2 promoted the expression of PTP4A1, a novel p53 target. GINS2 knockdown was increased, while PTP4A1 overexpression decreased the protein level of p53. Notably, PTP4A1 overexpression partly reversed the effects of GINS2 downregulation on colon cancer cells. Therefore, the present study demonstrated that GINS2 regulated the proliferation and apoptosis of colon cancer cells through PTP4A1/p53 pathway, highlighting that GINS2 may serve as a novel molecular marker for colon cancer prevention and therapy.