Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/104785
Title: Overexpression of CDC42SE1 in A431 cells reduced cell proliferation by inhibiting the Akt pathway
Authors: Kalailingam, Pazhanichamy
Tan, Hui Bing
Pan, Jiun Yit
Tan, Suat Hoon
Thanabalu, Thirumaran
Keywords: CDC42
Skin Cancer
DRNTU::Science::Biological sciences
Issue Date: 2019
Source: Kalailingam, P., Tan, H. B., Pan, J. Y., Tan, S. H., & Thanabalu, T. (2019). Overexpression of CDC42SE1 in A431 cells reduced cell proliferation by inhibiting the Akt pathway. Cells, 8(2), 117-. doi:10.3390/cells8020117
Series/Report no.: Cells
Abstract: Cell division cycle 42 (CDC42), a small Rho GTPase, plays a critical role in many cellular processes, including cell proliferation and survival. CDC42 interacts with the CRIB (Cdc42- and Rac-interactive binding) domain of CDC42SE1, a small effector protein of 9 kDa. We found that the expression of CDC42SE1 was reduced in human skin cancer samples relative to matched perilesional control. Exogenous expression of CDC42SE1 but not CDC42SE1H38A (mutation within CRIB domain) in A431 cells (A431SE1, A431SE1-H38A) reduced cell proliferation. Antibody microarray analysis of A431Ctrl and A431SE1 lysate suggested that reduced A431SE1 cells proliferation was due to inhibition of Akt pathway, which was confirmed by the reduced P-Akt and P-mTOR levels in A431SE1 cells compared to A431Ctrl cells. This suggests that CDC42SE1 modulates the CDC42-mediated Akt pathway by competing with other effector proteins to bind CDC42. A431SE1 cells formed smaller colonies in soft agar compared to A431Ctrl and A431SE1-H38A cells. These findings correlate with nude mice xenograft assays, where A431SE1 cells formed tumors with significantly-reduced volume compared to the tumors formed by A431Ctrl cells. Our results suggest that CDC42SE1 is downregulated in skin cancer to promote tumorigenesis, and thus CDC42SE1 might be an important marker of skin cancer progression.
URI: https://hdl.handle.net/10356/104785
http://hdl.handle.net/10220/48621
ISSN: 2073-4409
DOI: 10.3390/cells8020117
Rights: © 2019 The Author(s). Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SBS Journal Articles

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