ArticleOxidative medicine and cellular longevity2016
Inhibition of the RhoA GTPase Activity Increases Sensitivity of Melanoma Cells to UV Radiation Effects.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Molecular mechanisms of m6A modifications regulating tumor radioresistance.Molecular medicine (Cambridge, Mass.) · 2025Review
- Comprehensive analyses identify RIPOR2 as a genomic instability-associated immune prognostic biomarker in cervical cancer.Frontiers in immunology · 2022Article
- Skin Cancers and the Contribution of Rho GTPase Signaling Networks to Their Progression.Cancers · 2021Review
- Role of Small GTPase RhoA in DNA Damage Response.Biomolecules · 2021Review
- 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
- Subversion of Ras Small GTPases in Cutaneous Melanoma Aggressiveness.Frontiers in cell and developmental biology · 2020Review
- Low RhoA expression is associated with adverse outcome in melanoma patients: a clinicopathological analysis.American journal of translational research · 2019Article
- Actin cytoskeleton dynamics in stem cells from autistic individuals.Scientific reports · 2018Article
- Mechanisms and prevention of UV-induced melanoma.Photodermatology, photoimmunology & photomedicine · 2018Review
- Expression of Rho GTPases family in melanoma cells and its influence on cytoskeleton and migration.Oncotarget · 2017Article
- Impact of Silver Nanoparticles on the Ultraviolet Radiation Direct and Bystander Effects on TK6 Cell Line.Journal of medical physicsArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ultraviolet radiation is the main cause of DNA damage to melanocytes and development of melanoma, one of the most lethal human cancers, which leads to metastasis due to uncontrolled cell proliferation and migration. These phenotypes are mediated by RhoA, a GTPase overexpressed or overactivated in highly aggressive metastatic tumors that plays regulatory roles in cell cycle progression and cytoskeleton remodeling. This work explores whether the effects of UV on DNA damage, motility, proliferation, and survival of human metastatic melanoma cells are mediated by the RhoA pathway. Mutant cells expressing dominant-negative (MeWo-RhoA-N19) or constitutively active RhoA (MeWo-RhoA-V14) were generated and subjected to UV radiation. A slight reduction in migration and invasion was observed in MeWo and MeWo-RhoA-V14 cells but not in MeWo-RhoA-N19 cells, which presented inefficient motility and invasiveness associated with stress fibers fragmentation. Proliferation and survival of RhoA-deficient cells were drastically reduced by UV compared to cells displaying normal or high RhoA activity, suggesting increased sensitivity to UV. Loss of RhoA activity also caused less efficient DNA repair, with elevated levels of DNA lesions such as strand breaks and cyclobutane pyrimidine dimers (CPDs). Thus, RhoA mediates genomic stability and represents a potential target for sensitizing metastatic tumors to genotoxic agents.
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