Induction Of Cell Cycle Arrest By Increasing Gtp-Rhoa Levels Via Taxol-Induced Microtubule Polymerization In Renal Cell Carcinoma

Renal cell carcinoma (RCC) is the most common neoplasm of the kidney in adults, accounting for similar to 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.