Rev1, a member of the Y family polymerases, plays a key role in the translesion synthesis (TLS) pathway. TLS is an error - prone process that enables cells to overcome replication blockage caused by DNA damage. Rev1 has functions such as dCMP transferase activity and acts as a scaffolding protein for other TLS - involved polymerases [1,3]. The Rev1 - mutated mouse models, like the Rev1 transgenic (Tg) mouse model, are valuable research tools for studying Rev1's in vivo functions [1].

Rev1 - overexpressing (Rev1 - Tg) mice treated with N - methyl - N - nitrosourea (MNU) showed a higher incidence of intestinal adenoma, thymic lymphoma (TL), and increased mutagenesis in TL tumors compared to wild - type mice. Rev1 - Tg TLs had a higher mutation frequency, and pre - leukemic cells could be detected earlier in Rev1 - Tg mice after MNU treatment, suggesting that Rev1 overexpression accelerates mutagenesis and tumorigenesis by shortening the latency period [3]. In lung cancer, REV1 expression was upregulated in cancer tissues compared to adjacent tissues, and its silencing decreased the growth and proliferation of lung cancer cells. REV1 promoted lung carcinogenesis by upregulating SERTAD2 in a Rad18 - dependent manner, and a novel inhibitor JH - RE - 06 suppressed lung tumorigenesis [2].

In conclusion, Rev1 is essential in the TLS pathway, with a significant impact on mutagenesis and tumorigenesis. Mouse models, especially the Rev1 - Tg mice, have been crucial in revealing its role in cancer initiation and promotion, providing insights into the molecular mechanisms underlying these processes and potential therapeutic targets for cancer treatment [1,2,3].