ArticleMolecular and cellular biology2014
RhoB promotes γH2AX dephosphorylation and DNA double-strand break repair.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Plasma Proteomics of Type 2 Diabetes, Hypertension, and Co-Existing Diabetes/Hypertension in Thai Adults.Life (Basel, Switzerland) · 2024Article
- Statins in Cancer Prevention and Therapy.Cancers · 2023Review
- Genome resequencing clarifies phylogeny and reveals patterns of selection in the toxicogenomics modelPeerJ · 2022Article
- RHOAming Through the Nucleotide Excision Repair Pathway as a Mechanism of Cellular Response Against the Effects of UV Radiation.Frontiers in cell and developmental biology · 2020Article
- Dual Processing of R-Loops and Topoisomerase I Induces Transcription-Dependent DNA Double-Strand Breaks.Cell reports · 2019Article
- Regulation of RhoB Gene Expression during Tumorigenesis and Aging Process and Its Potential Applications in These Processes.Cancers · 2019Review
- PARP-1-dependent RND1 transcription induced by topoisomerase I cleavage complexes confers cellular resistance to camptothecin.Cell death & disease · 2018Article
- The RhoB small GTPase in physiology and disease.Small GTPases · 2018Review
- RHOB expression controls the activity of serine/threonine protein phosphatase PP2A to modulate mesenchymal phenotype and invasion in non-small cell lung cancers.Small GTPases · 2018Review
- Radiation-induced unrepairable DSBs: their role in the late effects of radiation and possible applications to biodosimetry.Journal of radiation research · 2018Review
- LB-100, a novel Protein Phosphatase 2A (PP2A) inhibitor, sensitizes malignant meningioma cells to the therapeutic effects of radiation.Cancer letters · 2018Article
- High-content tripartite split-GFP cell-based assays to screen for modulators of small GTPase activation.Journal of cell science · 2018Article
- Rgf1p (Rho1p GEF) is required for double-strand break repair in fission yeast.Nucleic acids research · 2017Article
- The RAS-related GTPase RHOB confers resistance to EGFR-tyrosine kinase inhibitors in non-small-cell lung cancer via an AKT-dependent mechanism.EMBO molecular medicine · 2017Article
- IER5 is involved in DNA Double-Strand Breaks Repair in Association with PAPR1 in Hela Cells.International journal of medical sciences · 2017Article
- The p53 isoform delta133p53ß regulates cancer cell apoptosis in a RhoB-dependent manner.PloS one · 2017Article
- Article
- Do DNA Double-Strand Breaks Drive Aging?Molecular cell · 2016Review
- RhoB loss induces Rac1-dependent mesenchymal cell invasion in lung cells through PP2A inhibition.Oncogene · 2016Article
- Radioresistance of Brain Tumors.Cancers · 2016Review
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Unlike other Rho GTPases, RhoB is rapidly induced by DNA damage, and its expression level decreases during cancer progression. Because inefficient repair of DNA double-strand breaks (DSBs) can lead to cancer, we investigated whether camptothecin, an anticancer drug that produces DSBs, induces RhoB expression and examined its role in the camptothecin-induced DNA damage response. We show that in camptothecin-treated cells, DSBs induce RhoB expression by a mechanism that depends notably on Chk2 and its substrate HuR, which binds to RhoB mRNA and protects it against degradation. RhoB-deficient cells fail to dephosphorylate γH2AX following camptothecin removal and show reduced efficiency of DSB repair by homologous recombination. These cells also show decreased activity of protein phosphatase 2A (PP2A), a phosphatase for γH2AX and other DNA damage and repair proteins. Thus, we propose that DSBs activate a Chk2-HuR-RhoB pathway that promotes PP2A-mediated dephosphorylation of γH2AX and DSB repair. Finally, we show that RhoB-deficient cells accumulate endogenous γH2AX and chromosomal abnormalities, suggesting that RhoB loss increases DSB-mediated genomic instability and tumor progression.
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