Home Blog of Signal Transduction Cell Cycle DNA/RNA Synthesis REV1 promotes lung tumorigenesis by activating the Rad18/SERTAD2 axis

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REV1 promotes lung tumorigenesis by activating the Rad18/SERTAD2 axis

REV1 is the central member of the family of TLS polymerases, which participate in various DNA damage repair and tolerance pathways and play a significant role in maintaining genomic stability. However, the role of REV1 in tumors is rarely reported. In this study, we found that the expression of REV1 was significantly upregulated in lung cancer tissues compared with matched adjacent tissues and was associated with poor prognosis. Functional experiments demonstrated that REV1 silencing decreased the growth and proliferation capacity of lung cancer cells. Mechanistically, REV1 upregulated the expression of SERTAD2 in a Rad18-dependent manner, thereby promoting lung carcinogenesis. A novel REV1 inhibitor, JH-RE-06, suppressed lung tumorigenesis in vivo and in vitro and was shown to be safe and well tolerated. Our study confirmed that REV1 is a potential diagnostic marker and therapeutic target for lung cancer and that JH-RE-06 may be a safe and efficient therapeutic agent for NSCLC.

 

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The passage you provided describes a study that investigated the role of REV1, a member of the TLS polymerase family, in lung cancer. The researchers observed that REV1 expression was significantly higher in lung cancer tissues compared to adjacent healthy tissues and that increased REV1 expression was associated with a poor prognosis. Functional experiments revealed that silencing REV1 in lung cancer cells led to decreased cell growth and proliferation.

The study also investigated the underlying mechanisms of REV1's role in lung carcinogenesis. It was found that REV1 upregulated the expression of SERTAD2 in a Rad18-dependent manner, which contributed to the promotion of lung cancer development.

Additionally, the researchers identified a novel REV1 inhibitor called JH-RE-06. This inhibitor was effective in suppressing lung tumor growth both in in vivo and in vitro experiments. Importantly, JH-RE-06 demonstrated safety and tolerability in the study.

Based on these findings, the study concludes that REV1 could serve as a potential diagnostic marker and therapeutic target for lung cancer. Furthermore, the novel REV1 inhibitor, JH-RE-06, shows promise as a safe and effective therapeutic agent for non-small cell lung cancer (NSCLC).

Related Products

Cat.No. Product Name Information
S8850 JH-RE-06 JH-RE-06 is a potent REV1-REV7 interface inhibitor with an IC50 of 0.78 μM and Kd value of 0.42 μM, disrupting REV1-POL ζ-mediated mutagenic translesion synthesis (TLS).

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DNA/RNA Synthesis