RNF113A as a poor prognostic factor promotes metastasis and invasion of CC through miR197/PRP19/P38MAPK signaling pathway

Abstract It has been demonstrated that aberrant expression of RNF113A plays a significant role in multiple diseases, including X-linked trichothiodystrophy syndrome, hepatocellular carcinoma, and esophageal cancer. However, the functional role of RNF113A in cervical cancer (CC) remains unclear. Thus, this study aimed to investigate the role of RNF113A in the development and prognosis of CC. For this purpose, sixty cases were included in the follow-up study. It was found that RNF113A protein was significantly up-regulated in CC tissues than in paired paracancerous tissues, and a high RNF113A expression was closely related to malignant phenotypes (differentiation degree, FIGO stage, depth of invasion, and lymph node metastasis). Meanwhile, RNF113A was found to be an independent risk factor affecting patients' prognosis, and those with high expression had a short survival period. To investigate the cause and mechanism of poor prognosis caused by RNF113A, functional studies were performed in vitro and in vivo by cell transfection, scratch wound healing assay, transwell assay, flow cytometry analysis, and tumor transplantation in nude mice. Interestingly, the results showed that RNF113A promoted migration and invasion and inhibited the apoptosis of CC cells contributing to poor prognosis. Mechanistically, RNF113A regulated the progression and prognosis of CC through the miR197/Prp19/p38Mark signaling pathway. Overall, our findings highlight the potential clinical implications of RNF113A as a poor prognostic factor in CC.