Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.ygyno.2012.06.039
Title: 14-3-3σ mediates G2-M arrest produced by 5-aza-2′-deoxycytidine and possesses a tumor suppressor role in endometrial carcinoma cells
Authors: Steiner, M.
Clark, B.
Tang, J.-Z.
Zhu, T.
Lobie, P.E. 
Keywords: 14-3-3sigma (stratifin SFN)
DAC-5-aza-2′ deoxycytidine
Endometrial cancer EC
G2-M cell cycle progression inhibition
Gene methylation
Issue Date: Oct-2012
Citation: Steiner, M., Clark, B., Tang, J.-Z., Zhu, T., Lobie, P.E. (2012-10). 14-3-3σ mediates G2-M arrest produced by 5-aza-2′-deoxycytidine and possesses a tumor suppressor role in endometrial carcinoma cells. Gynecologic Oncology 127 (1) : 231-240. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ygyno.2012.06.039
Abstract: Objectives: To determine the effect of 5-aza-2′-deoxycytidine (DAC) on human endometrial carcinoma cell (HECC) oncogenicity and demonstrate a molecular mechanism by which DAC modulates HECC oncogenicity. Methods: The effect of DAC was tested on HECC RL95-2, AN3, Ishikawa and ECC1 cells. The role of 14-3-3σ on HECC oncogenicity in response to DAC treatment was evaluated in RL95-2 and AN3 cells after forced expression or silencing of 14-3-3σ gene expression. Results: Treatment of HECC with DAC produced non-cytotoxic cell growth inhibition and G2/M cell cycle arrest. This effect was strongly correlated with increased expression of p21 and 14-3-3σ. Silencing of 14-3-3σ induced cellular proliferation and reduced the effect of DAC on cell cycle arrest in G2/M phases. Conversely, forced expression of 14-3-3σ showed the opposite effect. Furthermore, forced expression of 14-3-3σ in human endometrial cell lines reduced cell growth and colony formation. Conclusions: We suggest that 14-3-3σ in HECC suppresses cell proliferation and mediates DAC induced G2/M arrest and inhibition of cell proliferation in HECC. © 2012 Elsevier Inc.
Source Title: Gynecologic Oncology
URI: http://scholarbank.nus.edu.sg/handle/10635/109133
ISSN: 00908258
DOI: 10.1016/j.ygyno.2012.06.039
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