ArticleCell death & disease2022
REV1 promotes lung tumorigenesis by activating the Rad18/SERTAD2 axis.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 29 citations in OpenAlex.
- RAD18 facilitates cancer progression and immunosuppression via the AKT/mTOR/c-Myc axis: a multi-omics analysis.NPJ precision oncology · 2026Article
- REV1‑targeting inhibitor JH‑RE‑06 induces ferroptosis via NCOA4‑mediated ferritinophagy in colorectal cancer cells.Oncology reports · 2025Article
- Versatile enhancement of the killing potential of anti-cancer agents achieved by peptide mimetics of the PCNA interface towards specialized DNA polymerases.Cell death & disease · 2025Article
- Advances of E3 ligases in lung cancer.Biochemistry and biophysics reports · 2024Review
- USP9X-mediated REV1 deubiquitination promotes lung cancer radioresistance via the action of REV1 as a Rad18 molecular scaffold for cystathionine γ-lyase.Journal of biomedical science · 2024Article
- Targeting FBXO22 enhances radiosensitivity in non-small cell lung cancer by inhibiting the FOXM1/Rad51 axis.Cell death & disease · 2024Article
- Biological features of fowl adenovirus serotype-4.Frontiers in cellular and infection microbiology · 2024Review
- Integrative analysis of the lncRNA-miRNA-mRNA interactions in smooth muscle cell phenotypic transitions.Frontiers in genetics · 2024Article
- Targeting diacylglycerol kinase α impairs lung tumorigenesis by inhibiting cyclin D3.Thoracic cancer · 2023Article
- The diagnostic significance of the ZNF gene family in pancreatic cancer: a bioinformatics and experimental study.Frontiers in genetics · 2023Article
- RAD18 opposes transcription-associated genome instability through FANCD2 recruitment.PLoS genetics · 2022Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
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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