ArticleMolecular cancer research : MCR2009
REV1 is implicated in the development of carcinogen-induced lung cancer.
Article in Molecular cancer research : MCR, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Rev1 overexpression accelerates N-methyl-N-nitrosourea (MNU)-induced thymic lymphoma by increasing mutagenesis.Cancer science · 2024Article
- Leveraging the replication stress response to optimize cancer therapy.Nature reviews. Cancer · 2023Review
- REV1 promotes lung tumorigenesis by activating the Rad18/SERTAD2 axis.Cell death & disease · 2022Article
- Consequences of exposure to pollutants on respiratory health: From genetic correlations to causal relationships.PloS one · 2022Article
- REV1: A novel biomarker and potential therapeutic target for various cancers.Frontiers in genetics · 2022Article
- Manganese Is a Strong Specific Activator of the RNA Synthetic Activity of Human Polη.International journal of molecular sciences · 2021Article
- Genetic evaluation of the variants using MassARRAY in non-small cell lung cancer among North Indians.Scientific reports · 2021Article
- Making Choices: DNA Replication Fork Recovery Mechanisms.Seminars in cell & developmental biology · 2021Review
- Structures of REV1 UBM2 Domain Complex with Ubiquitin and with a Small-Molecule that Inhibits the REV1 UBM2-Ubiquitin Interaction.Journal of molecular biology · 2018Article
- Structural Basis for the Interaction of Mutasome Assembly Factor REV1 with Ubiquitin.Journal of molecular biology · 2018Article
- Small-molecules that bind to the ubiquitin-binding motif of REV1 inhibit REV1 interaction with K164-monoubiquitinated PCNA and suppress DNA damage tolerance.Bioorganic & medicinal chemistry · 2018Article
- BPDE-induced genotoxicity: relationship between DNA adducts, mutagenicity in the in vitro PIG-A assay, and the transcriptional response to DNA damage in TK6 cells.Archives of toxicology · 2018Article
- Rev1 contributes to proper mitochondrial function via the PARP-NADScientific reports · 2017Article
- Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy?PLoS genetics · 2017Review
- Article
- Starvation promotes REV1 SUMOylation and p53-dependent sensitization of melanoma and breast cancer cells.Cancer research · 2015Article
- Both high-fidelity replicative and low-fidelity Y-family polymerases are involved in DNA rereplication.Molecular and cellular biology · 2015Article
- Role of selected genetic variants in lung cancer risk in African Americans.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2013Article
- Structure and functional analysis of the BRCT domain of translesion synthesis DNA polymerase Rev1.Biochemistry · 2013Article
- Structural insights into the assembly of human translesion polymerase complexes.Protein & cell · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The somatic mutation hypothesis of cancer predicts that reducing the frequency of mutations induced by carcinogens will reduce the incidence of cancer. To examine this, we developed an antimutator strategy based on the manipulation of the level of a protein required for mutagenic bypass of DNA damage induced by the ubiquitous carcinogen benzo[a]pyrene. The expression of this protein, REV1, was reduced in mouse cells using a vector encoding a gene-specific targeting ribozyme. In the latter cells, mutagenesis induced by the activated form of benzo[a]pyrene was reduced by >90%. To examine if REV1 transcripts could be lowered in vivo, the plasmid was complexed with polyethyleneimine, a nonviral cationic polymer, and delivered to the lung via aerosol. The endogenous REV1 transcript in the bronchial epithelium as determined by quantitative real-time PCR in laser capture microdissected cells was reduced by 60%. There was a significant decrease in the multiplicity of carcinogen-induced lung tumors from 6.4 to 3.7 tumors per mouse. Additionally, REV1 inhibition completely abolished tumor formation in 27% of the carcinogen-exposed mice. These data support the central role of the translesion synthesis pathway in the development of lung cancer. Further, the selective modulation of members of this pathway presents novel potential targets for cancer prevention. The somatic mutation hypothesis of cancer predicts that the frequency of cancers will also be reduced.
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