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Distinct Roles for Rho Versus Rac/Cdc42 GTPases Downstream of Vav2 in Regulating Mammary Epithelial Acinar Architecture

Duan, Lei, Chen, Gengsheng, Virmani, Sumeet, Ying, GuoGuang, Raja, Srikumar M., Chung, Byung Min, Rainey, Mark A., Dimri, Manjari, Ortega-Cava, Cesar F., Zhao, Xiangshan, Clubb, Robert J., Tu, Chun, Reddi, Alagarsamy L., Naramura, Mayumi, Band, Vimla, Band, Hamid·2010·Journal of Biological Chemistry
DOI 10.1074/jbc.m109.057976
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Abstract

Non-malignant mammary epithelial cells (MECs) undergo acinar morphogenesis in three-dimensional Matrigel culture, a trait that is lost upon oncogenic transformation. Rho GTPases are thought to play important roles in regulating epithelial cell-cell junctions, but their contributions to acinar morphogenesis remain unclear. Here we report that the activity of Rho GTPases is down-regulated in non-malignant MECs in three-dimensional culture with particular suppression of Rac1 and Cdc42. Inducible expression of a constitutively active form of Vav2, a Rho GTPase guanine nucleotide exchange factor activated by receptor tyrosine kinases, in three-dimensional MEC culture activated Rac1 and Cdc42; Vav2 induction from early stages of culture impaired acinar morphogenesis, and induction in preformed acini disrupted the pre-established acinar architecture and led to cellular outgrowths. Knockdown studies demonstrated that Rac1 and Cdc42 mediate the constitutively active Vav2 phenotype, whereas in contrast, RhoA knockdown intensified the Vav2-induced disruption of acini, leading to more aggressive cell outgrowth and branching morphogenesis. These results indicate that RhoA plays an antagonistic role to Rac1/Cdc42 in the control of mammary epithelial acinar morphogenesis.

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  • 16A5 is a nontumorigenic, HPV16 E6/E7-immortalized, EGF-dependent human mammary epithelial cell line that displays expected ligand-induced EGFR degradation kinetics.

    “16A5 is a nontumorigenic, human papillomavirus 16 (HPV16) E6/E7-immortalized and EGF-dependent human mammary epithelial cell (MEC) line (55) that displays the expected ligand-induced EGFR degradation kinetics (56–60) (Fig. 1A).”

    From EHD1 and RUSC2 Control Basal Epidermal Growth Factor Receptor Cell Surface Expression and Recycling (2020) · cites this paper as [58]

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Metadata

Authors
Duan, L., Chen, G., Virmani, S., Ying, G., Raja, S. M., Chung, B. M., Rainey, M. A., Dimri, M., Ortega-Cava, C. F., Zhao, X., Clubb, R. J., Tu, C., Reddi, A. L., Naramura, M., Band, V., & Band, H.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2010-01
Volume
285
Issue
2
Pages
1555-1568
ISSN
0021-9258
DOI
10.1074/jbc.m109.057976
Cited by
23
References
2
Language
en
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