REV1 promotes lung tumorigenesis by activating the Rad18/SERTAD2 axis

REV1 is a vital family member of TLS polymerases, which take part in various DNA damage repair and tolerance pathways and play a substantial role to maintain genomic stability. However, the function of REV1 in tumors isn’t reported. Within this study, we discovered that the expression of REV1 was considerably upregulated in cancer of the lung tissues in contrast to matched adjacent tissues and it was connected with poor prognosis. Functional experiments shown that REV1 silencing decreased the development and proliferation capacity of cancer of the lung cells. Mechanistically, REV1 upregulated the expression of SERTAD2 inside a Rad18-dependent manner, therefore promoting lung carcinogenesis. A singular REV1 inhibitor, JH-RE-06, covered up lung tumorigenesis in vivo as well as in vitro and it was proven safe and well tolerated. Our study confirmed that REV1 is really a potential diagnostic marker and therapeutic target for cancer of the lung which JH-RE-06 can be a efficient and safe therapeutic agent for NSCLC.