ArticleMolecular cancer2012
MutS homologue hMSH5: role in cisplatin-induced DNA damage response.
Article in Molecular cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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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
16 citing papers in PubMed, 25 citations in OpenAlex.
- Aberrant DNA damage response pathways may predict the outcome of platinum chemotherapy in ovarian cancer.PloS one · 2015Trial
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- Methyltransferase-Like 3 Inhibition-Activated cGAS/STING Axis Enhances Immunotherapy and Poly(ADP-Ribose) Polymerase Inhibitor Sensitivity in Lung Adenocarcinoma.Research (Washington, D.C.) · 2026Article
- ATP6V1B1 regulates ovarian cancer progression and cisplatin sensitivity through the mTOR/autophagy pathway.Molecular and cellular biochemistry · 2025Article
- Transgenerational Epigenetic DNA Methylation Editing and Human Disease.Biomolecules · 2023Review
- Article
- TTK inhibition increases cisplatin sensitivity in high-grade serous ovarian carcinoma through the mTOR/autophagy pathway.Cell death & disease · 2021Article
- MicroRNA-765 sensitizes osteosarcoma cells to cisplatin via downregulating APE1 expression.OncoTargets and therapy · 2019Article
- A Decade of GWAS Results in Lung Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018Review
- Real-time monitoring of cisplatin cytotoxicity on three-dimensional spheroid tumor cells.Drug design, development and therapy · 2016Article
- hMSH5 Facilitates the Repair of Camptothecin-induced Double-strand Breaks through an Interaction with FANCJ.The Journal of biological chemistry · 2015Article
- DNA damage induced MutS homologue hMSH4 acetylation.International journal of molecular sciences · 2013Article
- Pro-crossover factors regulate damage-dependent apoptosis in the Caenorhabditis elegans germ line.Cell death and differentiation · 2013Article
- MutS homologue hMSH4: interaction with eIF3f and a role in NHEJ-mediated DSB repair.Molecular cancer · 2013Article
- MutS Homologues hMSH4 and hMSH5: Genetic Variations, Functions, and Implications in Human Diseases.Current genomics · 2013Article
- MutS homologue hMSH5: recombinational DSB repair and non-synonymous polymorphic variants.PloS one · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCisplatin (cis-diamminedichloroplatinum (II), CDDP) and its analogues constitute an important class of anticancer drugs in the treatment of various malignancies; however, its effectiveness is frequently affected by mutations in genes involved in the repair and signaling of cisplatin-induced DNA damage. These observations necessitate a need for a better understanding of the molecular events governing cellular sensitivity to cisplatin.
resultsHere, we show that hMSH5 mediates sensitization to cisplatin-induced DNA damage in human cells. Our study indicates that hMSH5 undergoes cisplatin-elicited protein induction and tyrosine phosphorylation. Silencing of hMSH5 by RNAi or expression of hMSH5 phosphorylation-resistant mutant hMSH5Y742F elevates cisplatin-induced G2 arrest and renders cells susceptible to cisplatin toxicity at clinically relevant doses. In addition, our data show that cisplatin promotes hMSH5 chromatin association and hMSH5 deficiency increases cisplatin-triggered γ-H2AX foci. Consistent with a possible role for hMSH5 in recombinational repair of cisplatin-triggered double-strand breaks (DSBs), the formation of cisplatin-induced hMSH5 nuclear foci is hRad51-dependent.
conclusionCollectively, our current study has suggested a role for hMSH5 in the processing of cisplatin-induced DSBs, and silencing of hMSH5 may provide a new means to improve the therapeutic efficacy of cisplatin.
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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 Socratic graph.