ArticleBreast cancer research : BCR2012
RAC1 GTPase plays an important role in γ-irradiation induced G2/M checkpoint activation.
Article in Breast cancer research : BCR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed, 62 citations in OpenAlex.
- Rac1 GTPase Regulates the SCFCancers · 2026Article
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- Effect of radiotherapy on the DNA cargo and cellular uptake mechanisms of extracellular vesicles.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023Review
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- Förster resonance energy transfer biosensors for fluorescence and time-gated luminescence analysis of rac1 activity.Scientific reports · 2022Article
- Cell Signaling Pathways That Promote Radioresistance of Cancer Cells.Diagnostics (Basel, Switzerland) · 2022Review
- CircRNA: A novel potential strategy to treat thyroid cancer (Review).International journal of molecular medicine · 2021Review
- Effects of MLL5 and HOXA regulated by NRP1 on radioresistance in A549.Oncology letters · 2021Article
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- Modulating the Radiation Response for Improved Outcomes in Breast Cancer.JCO precision oncology · 2021Review
- Rho GTPases in cancer radiotherapy and metastasis.Cancer metastasis reviews · 2020Review
- Rho GTPases: Big Players in Breast Cancer Initiation, Metastasis and Therapeutic Responses.Cells · 2020Review
- Invasion inhibition in pancreatic cancer using the oral iron chelating agent deferasirox.BMC cancer · 2020Article
- PARP-1-dependent RND1 transcription induced by topoisomerase I cleavage complexes confers cellular resistance to camptothecin.Cell death & disease · 2018Article
- Targeting Rac and Cdc42 GTPases in Cancer.Cancer research · 2018Review
- Silencing Ras-Related C3 Botulinum Toxin Substrate 1 Inhibits Growth and Migration of Hypopharyngeal Squamous Cell Carcinoma via the P38 Mitogen-Activated Protein Kinase Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- The R-Enantiomer of Ketorolac Delays Mammary Tumor Development in Mouse Mammary Tumor Virus-Polyoma Middle T Antigen (MMTV-PyMT) Mice.The American journal of pathology · 2018Article
- Rho inhibition by lovastatin affects apoptosis and DSB repair of primary human lung cells in vitro and lung tissue in vivo following fractionated irradiation.Cell death & disease · 2017Article
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5 authors at 2 institutions in 1 country.
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Abstract
introductionIn response to gamma-irradiation (IR)-induced double-strand DNA breaks, cells undergo cell-cycle arrest, allowing time for DNA repair before reentering the cell cycle. G2/M checkpoint activation involves activation of ataxia telangiectasia mutated (ATM)/ATM- and rad3-related (ATR) kinases and inhibition of Cdc25 phosphatases, resulting in inhibition of Cdc2 kinase and subsequent G2/M cell-cycle arrest. Previous studies from our laboratory showed that the G2/M checkpoint activation after IR exposure of MCF-7 breast cancer cells is dependent on the activation of extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) signaling. In the present studies, we investigated the role of Ras-related C3 botulinum toxin substrate 1 (Rac1) guanosine triphosphatase (GTPase) in IR-induced G2/M checkpoint response and ERK1/2 activation, as well as in cell survival after IR.
methodsWith Rac1-specific inhibitor, dominant negative mutant Rac1 (N17Rac1) and specific small interfering RNA, the effect of Rac1 on IR-induced G2/M checkpoint response and ERK1/2 activation was examined in human breast cancer cells. In addition, the effect of Rac1 on cell survival after irradiation was assessed by using Rac1-specific inhibitor.
resultsIR exposure of MCF-7 breast cancer cells was associated with a marked activation of Rac1 GTPase. Furthermore, inhibition of Rac1 by using specific inhibitor, dominant-negative Rac1 mutant, or specific siRNA resulted in attenuation of IR-induced G2/M arrest and concomitant diminution of IR-induced activation of ATM, ATR, Chk1, and Chk2 kinases, as well as phosphorylation of Cdc2-Tyr15. Moreover, Rac1 inhibition or decreased Rac1 expression also abrogated IR-induced phosphorylation of mitogen-activated protein kinase kinase 1 and 2 (MEK1/2) and ERK1/2. Ultimately, inhibition of Rac1 markedly increased cellular sensitivity to IR exposure, which involves induction of apoptosis.
conclusionStudies in this report suggest that Rac1 GTPase plays an essential role in the activation of IR-induced ERK1/2 signaling and subsequent G2/M checkpoint response. Furthermore, results also support a role for Rac1 in promoting cell survival after irradiation treatment.
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