ArticleMolecular medicine reports2017
Induction of cell cycle arrest by increasing GTP‑RhoA levels via Taxol‑induced microtubule polymerization in renal cell carcinoma.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 12 citations in OpenAlex.
- Review
- Paclitaxel induces NM2-dependent cellular contraction through GEF-H1 dissociation from microtubules and RhoA/ROCK activation in cancer cells.Molecular oncology · 2026Article
- Optical blood-brain-tumor barrier modulation expands therapeutic options for glioblastoma treatment.Nature communications · 2023Article
- Successful first-line treatment of simultaneous multiple primary malignancies of lung adenocarcinoma and renal clear cell carcinoma: A case report.Frontiers in immunology · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
Renal cell carcinoma (RCC) is the most common neoplasm of the kidney in adults, accounting for ~3% of adult malignancies. Understanding the underlying mechanism of RCC tumorigenesis is necessary to improve patient survival. The present study revealed that Taxol‑induced microtubule (MT) polymerization causes cell cycle arrest and an increase in guanosine triphosphate‑Ras homology gene family, member A (GTP‑RhoA) protein expression. Disruption of Taxol‑induced MT polymerization reversed GTP‑RhoA expression and cell cycle arrest. The localization and redistribution of MTs and RhoA were consistent in cells with MT bundles and those without. Decreased GTP‑RhoA had no marked effect on Taxol‑induced MT bundling, however, it reduced the proportion of cells in G2/M phase. Taken together, Taxol‑induced MT polymerization regulated the protein expression levels of GTP‑RhoA and cell cycle arrest. However, the alteration in GTP‑RhoA expression did not influence MT arrangement, suggesting that GTP‑RhoA serves a pivotal role in Taxol‑induced MT polymerization and cell cycle arrest in RCC.
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