RESUMEN
The detailed molecular mechanisms underlying the carcinogenesis of colorectal carcinoma (CRC) remain unknown. Therefore, the present study was designed to investigate the effect of the relationship between C2ORF68 and HuR in regards to the carcinogenesis of CRC. Immunohistochemistry, immunofluorescence, flow cytometry, Transwell migration and CCK8 assays, coimmunoprecipitation, qRTPCR and western blot analysis were performed. The results revealed that expression of C2ORF68 was significantly upregulated in the cytoplasm and nucleus in rectal cancer, and upregulation of the expression of C2ORF68 was associated with lymph node metastasis and pathological grade. C2ORF68 and HuR were found to be mainly localized in the nucleus in both SW480 and LoVo cells. In LoVo+c2orf68,HuR and LoVo+c2orf68 cells, the cell apoptosis rate was significantly decreased, cell proliferation rate was significantly increased, and the cell migration rate was only significantly increased in the LoVo+c2orf68 cells. In SW480c2orf68,HuR, SW480c2orf68 and SW480HuR, the cell apoptosis rate was significantly increased. At the same time, cell proliferation and the cell migration rate were significantly decreased. The mRNA and protein expression levels of C2orf68, HuR, Bcl2, cMyc, cyclin D and cyclin A were upregulated, while the expression of Bax was downregulated in LoVo+c2orf68 and LoVo+c20rf68,HuR cells. Expression levels of C2orf68, HuR, Bcl2, cMyc, cyclin D and cyclin A were downregulated while Bax was upregulated in the SW480c2orf68,HuR, SW480c2orf68 and SW480HuR cells. In conclusion, it is suggested that c2orf68 is a potential carcinogenesis factor in rectal cancer. Furthermore, c2orf68 may have a synergistic effect with HuR in the onset and development of CRC.