ArticlePloS one2017
RAC1b overexpression stimulates proliferation and NF-kB-mediated anti-apoptotic signaling in thyroid cancer cells.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Long noncoding RNA FAM111A-DT promotes aggressiveness of papillary thyroid cancer via activating NF-κB signaling.Journal of endocrinological investigation · 2025Article
- An updated review summarizing the anticancer potential of flavonoids via targeting NF-kB pathway.Frontiers in pharmacology · 2024Review
- Emodin treatment of papillary thyroid cancer cell linesOncology letters · 2023Article
- Inflammatory Control of Viral Infection.Viruses · 2023Article
- The Role of Fast-Cycling Atypical RHO GTPases in Cancer.Cancers · 2022Review
- MAPK Inhibition Requires Active RAC1 Signaling to Effectively Improve Iodide Uptake by Thyroid Follicular Cells.Cancers · 2021Article
- Article
- Alternative Splicing: Expanding the Landscape of Cancer Biomarkers and Therapeutics.International journal of molecular sciences · 2020Review
- Inflammatory Microenvironment Modulation of Alternative Splicing in Cancer: A Way to Adapt.Advances in experimental medicine and biology · 2020Review
- TNFα-mediated activation of NF-κB downregulates sodium-iodide symporter expression in thyroid cells.PloS one · 2020Article
- RAC1B: A Rho GTPase with Versatile Functions in Malignant Transformation and Tumor Progression.Cells · 2019Review
- Alternative-splicing defects in cancer: Splicing regulators and their downstream targets, guiding the way to novel cancer therapeutics.Wiley interdisciplinary reviews. RNA · 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
- Influence of transcriptional variants on metastasis.RNA biology · 2018Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of tumor-associated RAC1b has been recently highlighted as one of the most promising targets for therapeutic intervention in colon, breast, lung and pancreatic cancer. RAC1b is a hyperactive variant of the small GTPase RAC1 and has been recently shown to be overexpressed in a subset of papillary thyroid carcinomas associated with unfavorable outcome. Using the K1 PTC derived cell line as an in vitro model, we observed that both RAC1 and RAC1b were able to induce a significant increase on NF-kB and cyclin D1 reporter activity. A clear p65 nuclear localization was found in cells transfected with RAC1b-WT, confirming NF-kB canonical pathway activation. Consistently, we observed a RAC1b-mediated decrease in IκBα (NF-kB inhibitor) protein levels. Moreover, we show that RAC1b overexpression stimulates G1/S progression and protects thyroid cells against induced apoptosis, the latter through a process involving the NF-kB pathway. Present data support previous findings suggesting an important role for RAC1b in the development of follicular cell-derived thyroid malignancies and point out NF-kB activation as one of the molecular mechanisms associated with the pro-tumorigenic advantage of RAC1b overexpression in thyroid carcinomas.
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