ArticleThe Journal of biological chemistry2015
Arsenic Inhibits DNA Mismatch Repair by Promoting EGFR Expression and PCNA Phosphorylation.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 43 citations in OpenAlex.
- Memory effects of prior subculture may impact the quality of multiomic perturbation profiles.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- Arsenic in brown rice: do the benefits outweigh the risks?Frontiers in nutrition · 2023Review
- Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023Article
- The mismatch recognition protein MutSα promotes nascent strand degradation at stalled replication forks.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Inhibition of ABL1 by tyrosine kinase inhibitors leads to a downregulation of MLH1 by Hsp70-mediated lysosomal protein degradation.Frontiers in genetics · 2022Article
- Chemopreventive Role of Black Tea Extract in Swiss Albino Mice Exposed to Inorganic Arsenic.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Arsenic co-carcinogenesis: Inhibition of DNA repair and interaction with zinc finger proteins.Seminars in cancer biology · 2021Review
- Epigenetic effects of low-level sodium arsenite exposure on human liver HepaRG cells.Archives of toxicology · 2020Article
- Chronic and acute arsenic exposure enhance EGFR expression via distinct molecular mechanisms.Toxicology in vitro : an international journal published in association with BIBRA · 2020Article
- HB-EGF Activates the EGFR/HIF-1α Pathway to Induce Proliferation of Arsenic-Transformed Cells and Tumor Growth.Frontiers in oncology · 2020Article
- Arsenic‑induced BRCA1 CpG promoter methylation is associated with the downregulation of ERα and resistance to tamoxifen in MCF7 breast cancer cells and mouse mammary tumor xenografts.International journal of oncology · 2019Article
- The Impact of Long-term Exposure to Low Levels of Inorganic Arsenic on the Hypomethylation of SEPT9 Promoter in Epithelial-Mesenchymal Transformed Colorectal Cancer Cell Lines.International journal of molecular and cellular medicine · 2019Article
- Epigenetics of breast cancer: Modifying role of environmental and bioactive food compounds.Molecular nutrition & food research · 2016Review
- Ubiquitin-specific Peptidase 10 (USP10) Deubiquitinates and Stabilizes MutS Homolog 2 (MSH2) to Regulate Cellular Sensitivity to DNA Damage.The Journal of biological chemistry · 2016Article
- Regulation of mismatch repair by histone code and posttranslational modifications in eukaryotic cells.DNA repair · 2016Review
- Regulation of therapeutic resistance in cancers by receptor tyrosine kinases.American journal of cancer research · 2016Article
- Identifying therapeutic targets in gastric cancer: the current status and future direction.Acta biochimica et biophysica Sinica · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Both genotoxic and non-genotoxic chemicals can act as carcinogens. However, while genotoxic compounds lead directly to mutations that promote unregulated cell growth, the mechanism by which non-genotoxic carcinogens lead to cellular transformation is poorly understood. Using a model non-genotoxic carcinogen, arsenic, we show here that exposure to arsenic inhibits mismatch repair (MMR) in human cells, possibly through its ability to stimulate epidermal growth factor receptor (EGFR)-dependent tyrosine phosphorylation of proliferating cellular nuclear antigen (PCNA). HeLa cells exposed to exogenous arsenic demonstrate a dose- and time-dependent increase in the levels of EGFR and tyrosine 211-phosphorylated PCNA. Cell extracts derived from arsenic-treated HeLa cells are defective in MMR, and unphosphorylated recombinant PCNA restores normal MMR activity to these extracts. These results suggest a model in which arsenic induces expression of EGFR, which in turn phosphorylates PCNA, and phosphorylated PCNA then inhibits MMR, leading to increased susceptibility to carcinogenesis. This study suggests a putative novel mechanism of action for arsenic and other non-genotoxic carcinogens.
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What OpenQuestion holds
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.