Background: Several Rho GTPase-activating proteins (RhoGAPs) are implicated in tumor progression through their effects on Rho GTPase activity. ARHGAP21 is a RhoGAP with increased expression in head and neck squamous cell carcinoma and with a possible role in glioblastoma tumor progression, yet little is known about the function of ARHGAP21 in cancer cells. Here we studied the role of ARHGAP21 in two prostate adenocarcinoma cell lines, LNCaP and PC3, which respectively represent initial and advanced stages of prostate carcinogenesis.

Results: ARHGAP21 is located in the nucleus and cytoplasm of both cell lines and its depletion resulted in decreased proliferation and increased migration of PC3 cells but not LNCaP cells. In PC3 cells, ARHGAP21 presented GAP activity for RhoA and RhoC and induced changes in cell morphology. Moreover, its silencing altered the expression of genes involved in cell proliferation and cytoskeleton organization, as well as the endothelin-1 canonical pathway.

Conclusions: Our results reveal new functions and signaling pathways regulated by ARHGAP21, and indicate that it could contribute to prostate cancer progression.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bbadis.2012.11.010DOI Listing

Publication Analysis

Top Keywords

arhgap21 rhogap
8
rhoa rhoc
8
prostate adenocarcinoma
8
tumor progression
8
cell lines
8
pc3 cells
8
arhgap21
7
cells
5
cell
5
rhogap rhoa
4

Similar Publications

Rho GTPase activating protein 21-mediated regulation of prostate cancer associated 3 gene in prostate cancer cell.

Braz J Med Biol Res

June 2024

Laboratório de Genética e Biotecnologia, Instituto de Biotecnologia, Universidade Federal de Uberlândia, Patos de Minas, MG, Brasil.

The overexpression of the prostate cancer antigen 3 (PCA3) gene is well-defined as a marker for prostate cancer (PCa) diagnosis. Although widely used in clinical research, PCA3 molecular mechanisms remain unknown. Herein we used phage display technology to identify putative molecules that bind to the promoter region of PCA3 gene and regulate its expression.

View Article and Find Full Text PDF

C. elegans Afadin is required for epidermal morphogenesis and functionally interfaces with the cadherin-catenin complex and RhoGAP PAC-1/ARHGAP21.

Dev Biol

July 2024

Department of Cell Biology, NYU School of Medicine, New York, NY, 10016, USA; Skirball Institute of Biomolecular Medicine, NYU School of Medicine, New York, NY, 10016, USA; University of Wisconsin - Madison, Department of Cell and Regenerative Biology and Center for Quantitative Cell Imaging, Madison, WI, 53706, USA. Electronic address:

During epithelial morphogenesis, the apical junctions connecting cells must remodel as cells change shape and make new connections with their neighbors. In the C. elegans embryo, new apical junctions form when epidermal cells migrate and seal with one another to encase the embryo in skin ('ventral enclosure'), and junctions remodel when epidermal cells change shape to squeeze the embryo into a worm shape ('elongation').

View Article and Find Full Text PDF

[ARHGAP21 inhibits epithelial-mesenchymal transition by inactivating the WNT signaling pathway in non-small cell lung cancer].

Nan Fang Yi Ke Da Xue Xue Bao

August 2023

Cancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510315, China.

Objective: To investigate the role of Rho GTPase-activating protein 21 (ARHGAP21) in regulating the migration and metastasis of non-small cell lung cancer (NSCLC) cells.

Methods: TCGA, CPTAC database were used to analyze the correlation of ARHGAP21 expression level in NSCLC and the patients' prognosis. The expression of ARHGAP21 in clinical specimens of NSCLC tissues was examined using Western blotting and immunohistochemistry.

View Article and Find Full Text PDF

YangXueQingNaoWan attenuated blood brain barrier disruption after thrombolysis with tissue plasminogen activator in ischemia stroke.

J Ethnopharmacol

January 2024

Department of Integration of Chinese and Western Medicine, School of Basic Medical Sciences, Peking University, Beijing 100191, China; Tasly Microcirculation Research Center, Peking University Health Science Center, Beijing 100191, China; Key Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People's Republic of China, Beijing 100191, China; Key Laboratory of Microcirculation, State Administration of Traditional Chinese Medicine of the People's Republic of China, Beijing 100191, China; State Key Laboratory of Core Technology in Innovative Chinese Medicine, Beijing 100191, China; The Key Discipline for Basic Integration of Chinese and Western Medicine (microcirculation) of the National Administration of Traditional Chinese Medicine, Beijing 100191, China. Electronic address:

Ethnopharmacological Relevant: YangXueQingNaoWan (YXQNW), a compound Chinese medicine, has been widely used for dizziness, irritability, insomnia, and dreaminess caused by blood deficiency and liver hyperactivity in China. However, whether YXQNW can inhibit cerebral microvascular exudation and cerebral hemorrhage (CH) caused by blood brain barrier (BBB) damage after tissue plasminogen activator (tPA) still unknown.

Aim Of The Research: To observe the effect of YXQNW on cerebral microvascular exudation and CH after tPA and investigate its mechanism in protecting BBB.

View Article and Find Full Text PDF

During epithelial morphogenesis, the apical junctions connecting cells must remodel as cells change shape and make new connections with their neighbors. In the embryo, new apical junctions form when epidermal cells migrate and seal with one another to encase the embryo in skin ('ventral enclosure'), and junctions remodel when epidermal cells change shape to squeeze the embryo into a worm shape ('elongation'). The junctional cadherin-catenin complex (CCC), which links epithelial cells to each other and to cortical actomyosin, is essential for epidermal morphogenesis.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!