ArticleNeoplasia (New York, N.Y.)2011
Inhibition of REV3 expression induces persistent DNA damage and growth arrest in cancer cells.
Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 58 citations in OpenAlex.
- REV1 Loss Triggers a G2/M Cell-Cycle Arrest Through Dysregulation of Mitotic Regulators.Genes · 2025Article
- A rapid method of evaluating cytotoxic drug efficacy using sub-cellular fluctuation imaging.Scientific reports · 2025Article
- LDHB silencing enhances the effects of radiotherapy by impairing nucleotide metabolism and promoting persistent DNA damage.Scientific reports · 2025Article
- Schedule-Dependent Treatment Increases Chemotherapy Efficacy in Malignant Pleural Mesothelioma.International journal of molecular sciences · 2022Article
- Implications of inhibition of Rev1 interaction with Y family DNA polymerases for cisplatin chemotherapy.Genes & development · 2021Article
- Chemotherapy-induced CDA expression renders resistant non-small cell lung cancer cells sensitive to 5'-deoxy-5-fluorocytidine (5'-DFCR).Journal of experimental & clinical cancer research : CR · 2021Article
- Site-specific proteolytic cleavage prevents ubiquitination and degradation of human REV3L, the catalytic subunit of DNA polymerase ζ.Nucleic acids research · 2020Article
- Identification of Prognostic miRNA Signature and Lymph Node Metastasis-Related Key Genes in Cervical Cancer.Frontiers in pharmacology · 2020Article
- MicroRNA‑29a enhances cisplatin sensitivity in non‑small cell lung cancer through the regulation of REV3L.Molecular medicine reports · 2019Article
- DNA polymerase ζ deficiency causes impaired wound healing and stress-induced skin pigmentation.Life science alliance · 2018Article
- Absence of REV3L promotes p53-regulated cancer cell metabolism in cisplatin-treated lung carcinoma cells.Biochemical and biophysical research communications · 2018Article
- MicroRNA-340 inhibits the proliferation and promotes the apoptosis of colon cancer cells by modulating REV3L.Oncotarget · 2018Article
- Live-Cell Mesothelioma Biobank to Explore Mechanisms of Tumor Progression.Frontiers in oncology · 2018Article
- Phosphorylation of ETS-1 is a critical event in DNA polymerase iota-induced invasion and metastasis of esophageal squamous cell carcinoma.Cancer science · 2017Article
- DNA polymerases in the mitochondria: A critical review of the evidence.Frontiers in bioscience (Landmark edition) · 2017Review
- Reversible p53 inhibition prevents cisplatin ototoxicity without blocking chemotherapeutic efficacy.EMBO molecular medicine · 2017Article
- Roles of human POLD1 and POLD3 in genome stability.Scientific reports · 2016Article
- Growth arrest of lung carcinoma cells (A549) by polyacrylate-anchored peroxovanadate by activating Rac1-NADPH oxidase signalling axis.Molecular and cellular biochemistry · 2016Article
- Article
- Exome sequencing reveals recurrent REV3L mutations in cisplatin-resistant squamous cell carcinoma of head and neck.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
REV3 is the catalytic subunit of DNA translesion synthesis polymerase ζ. Inhibition of REV3 expression increases the sensitivity of human cells to a variety of DNA-damaging agents and reduces the formation of resistant cells. Surprisingly, we found that short hairpin RNA-mediated depletion of REV3 per se suppresses colony formation of lung (A549, Calu-3), breast (MCF-7, MDA-MB-231), mesothelioma (IL45 and ZL55), and colon (HCT116 +/-p53) tumor cell lines, whereas control cell lines (AD293, LP9-hTERT) and the normal mesothelial primary culture (SDM104) are less affected. Inhibition of REV3 expression in cancer cells leads to an accumulation of persistent DNA damage as indicated by an increase in phospho-ATM, 53BP1, and phospho-H2AX foci formation, subsequently leading to the activation of the ATM-dependent DNA damage response cascade. REV3 depletion in p53-proficient cancer cell lines results in a G(1) arrest and induction of senescence as indicated by the accumulation of p21 and an increase in senescence-associated β-galactosidase activity. In contrast, inhibition of REV3 expression in p53-deficient cells results in growth inhibition and a G(2)/M arrest. A small fraction of the p53-deficient cancer cells can overcome the G(2)/M arrest, which results in mitotic slippage and aneuploidy. Our findings reveal that REV3 depletion per se suppresses growth of cancer cell lines from different origin, whereas control cell lines and a mesothelial primary culture were less affected. Thus, our findings indicate that depletion of REV3 not only can amend cisplatin-based cancer therapy but also can be applied for susceptible cancers as a potential monotherapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.