Downregulation of NIT2 inhibits colon cancer cell proliferation and induces cell cycle arrest through the caspase-3 and PARP pathways.

ABSTRACT

Colorectal cancer, also known as colon cancer is the most devastating malignancy worldwide. Previous studies have reported that Nit2, a member of the nitrilase superfamily, is a potential tumor suppressor, although its function remains elusive in colon cancer. In the present study, we employed an RNA interference lentivirus system to silence endogenous NIT2 expression in the colon cancer cell line, HCT116. The knockdown efficiency was determined by RT-qPCR and western blot analysis. The depletion of NIT2 markedly inhibited colon cancer cell proliferation and colony formation and induced cell cycle arrest in the G0/G1 phase, as shown by MTT assay, colony formation assay and flow cytometric analysis, respectively. Further investigation with an intracellular signaling array demonstrated that the depletion of NIT2 triggered the apoptosis of colon cancer cells through the caspase-3 and poly(ADP-ribose) polymerase (PARP) pathways. Our findings suggest that NIT2 may be an oncogene in human colon cancer and may thus serve as a promising therapeutic target for the treatment of colon cancer.