ArticleMolecular and cellular biochemistry2015
Rac1 GTPase-deficient HeLa cells present reduced DNA repair, proliferation, and survival under UV or gamma irradiation.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Rac1 GTPase Regulates the SCFCancers · 2026Article
- Somatic mutations in IRE1α regulate keratinocyte migration and survival by differentially activating Rho GTPases.Journal of cell science · 2025Article
- The effect and related mechanisms of RAC1 GTP on radiotherapy for hepatocellular carcinoma.Translational cancer research · 2025Article
- Downregulation of the Rho GTPase pathway abrogates resistance to ionizing radiation in wild-type p53 glioblastoma by suppressing DNA repair mechanisms.Cell death & disease · 2023Article
- Cell Signaling Pathways That Promote Radioresistance of Cancer Cells.Diagnostics (Basel, Switzerland) · 2022Review
- Long Noncoding RNAs Regulate the Radioresistance of Breast Cancer.Analytical cellular pathology (Amsterdam) · 2021Review
- Rho GTPases in cancer radiotherapy and metastasis.Cancer metastasis reviews · 2020Review
- DUSP3 maintains genomic stability and cell proliferation by modulating NER pathway and cell cycle regulatory proteins.Cell cycle (Georgetown, Tex.) · 2020Article
- 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
- The Rac1 splice form Rac1b favors mouse colonic mucosa regeneration and contributes to intestinal cancer progression.Oncogene · 2018Article
- PARP-1-dependent RND1 transcription induced by topoisomerase I cleavage complexes confers cellular resistance to camptothecin.Cell death & disease · 2018Article
- Epidermal Rac1 regulates the DNA damage response and protects from UV-light-induced keratinocyte apoptosis and skin carcinogenesis.Cell death & disease · 2017Article
- DOCK2 interacts with FLT3 and modulates the survival of FLT3-expressing leukemia cells.Leukemia · 2017Article
- RAC1 GTPase promotes the survival of breast cancer cells in response to hyper-fractionated radiation treatment.Oncogene · 2016Article
- Deletion of epidermal Rac1 inhibits HPV-8 induced skin papilloma formation and facilitates HPV-8- and UV-light induced skin carcinogenesis.Oncotarget · 2016Article
- Growth arrest of lung carcinoma cells (A549) by polyacrylate-anchored peroxovanadate by activating Rac1-NADPH oxidase signalling axis.Molecular and cellular biochemistry · 2016Article
- Inhibition of the RhoA GTPase Activity Increases Sensitivity of Melanoma Cells to UV Radiation Effects.Oxidative medicine and cellular longevity · 2016Article
- RAC1 overexpression promotes the proliferation, migration and epithelial-mesenchymal transition of lens epithelial cells.International journal of clinical and experimental pathology · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rac1 GTPase controls essential cellular functions related to the cytoskeleton, such as motility and adhesion. Rac1 is overexpressed in many tumor cells, including breast cancers, where it is also involved in the proliferation and checkpoint control necessary for the cell's recovery after exposure to ionizing radiation. However, its role in DNA damage and repair remains obscure in other tumor cells and under different genotoxic conditions. Here, we compare HeLa cells with mutants exogenously expressing a dominant-negative Rac1 (HeLa-Rac1-N17) by their responses to DNA damage induced by gamma or UV radiation. In HeLa cells, these treatments led to increased levels of active Rac1 (Rac1-GTP) and of stress fibers, with a diminished ability to migrate compared to untreated cells. However, the reduction of Rac1-GTP in Rac1-N17-deficient clones resulted in much higher levels of polymerized stress fibers accompanied by a strong impairment of cell migration, even after both radiation treatments. With regard to proliferation and genomic stability, dominant-negative Rac1 cells were more sensitive to gamma and UV radiation, exhibiting reduced proliferation and survival consistent with increased DNA damage and delayed or reduced DNA repair observed in this Rac1-deficient clone. The DNA damage response, as indicated by pH2AX and pChk1 levels, was increased in HeLa cells but was not effectively triggered in the Rac1-N17 clone after radiation treatment, which is likely the main cause of DNA damage accumulation. These data suggest that Rac1 GTPase plays an important role in signaling and contributes to the sensitivity of cervical cancer cells under UV or gamma radiation treatments.
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