14-3-3{sigma} mediates G2-M arrest produced by 5-aza-2'-deoxycytidine and possesses a tumor suppressor role in endometrial carcinoma cells

Michael Steiner, Brett Clark, Jian-Zhong Tang, Tao Zhu, Peter E Lobie

Research output: Contribution to journalArticleResearchpeer-review

4 Citations (Scopus)

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 14-3-3sigma on HECC oncogenicity in response to DAC treatment was evaluated in RL95-2 and AN3 cells after forced expression or silencing of 14-3-3sigma 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 14-3-3sigma. Silencing of 14-3-3sigma induced cellular proliferation and reduced the effect of DAC on cell cycle arrest in G2/M phases. Conversely, forced expression of 14-3-3sigma showed the opposite effect. Furthermore, forced expression of 14-3-3sigma in human endometrial cell lines reduced cell growth and colony formation. CONCLUSIONS: We suggest that 14-3-3sigma in HECC suppresses cell proliferation and mediates DAC induced G2/M arrest and inhibition of cell proliferation in HECC.
Original languageEnglish
Pages (from-to)231 - 240
Number of pages10
JournalGynecologic Oncology
Volume127
Issue number1
DOIs
Publication statusPublished - 2012

Cite this

Steiner, Michael ; Clark, Brett ; Tang, Jian-Zhong ; Zhu, Tao ; Lobie, Peter E. / 14-3-3{sigma} mediates G2-M arrest produced by 5-aza-2'-deoxycytidine and possesses a tumor suppressor role in endometrial carcinoma cells. In: Gynecologic Oncology. 2012 ; Vol. 127, No. 1. pp. 231 - 240.
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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 14-3-3sigma on HECC oncogenicity in response to DAC treatment was evaluated in RL95-2 and AN3 cells after forced expression or silencing of 14-3-3sigma 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 14-3-3sigma. Silencing of 14-3-3sigma induced cellular proliferation and reduced the effect of DAC on cell cycle arrest in G2/M phases. Conversely, forced expression of 14-3-3sigma showed the opposite effect. Furthermore, forced expression of 14-3-3sigma in human endometrial cell lines reduced cell growth and colony formation. CONCLUSIONS: We suggest that 14-3-3sigma in HECC suppresses cell proliferation and mediates DAC induced G2/M arrest and inhibition of cell proliferation in HECC.",
author = "Michael Steiner and Brett Clark and Jian-Zhong Tang and Tao Zhu and Lobie, {Peter E}",
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14-3-3{sigma} mediates G2-M arrest produced by 5-aza-2'-deoxycytidine and possesses a tumor suppressor role in endometrial carcinoma cells. / Steiner, Michael; Clark, Brett; Tang, Jian-Zhong; Zhu, Tao; Lobie, Peter E.

In: Gynecologic Oncology, Vol. 127, No. 1, 2012, p. 231 - 240.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - 14-3-3{sigma} mediates G2-M arrest produced by 5-aza-2'-deoxycytidine and possesses a tumor suppressor role in endometrial carcinoma cells

AU - Steiner, Michael

AU - Clark, Brett

AU - Tang, Jian-Zhong

AU - Zhu, Tao

AU - Lobie, Peter E

PY - 2012

Y1 - 2012

N2 - 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 14-3-3sigma on HECC oncogenicity in response to DAC treatment was evaluated in RL95-2 and AN3 cells after forced expression or silencing of 14-3-3sigma 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 14-3-3sigma. Silencing of 14-3-3sigma induced cellular proliferation and reduced the effect of DAC on cell cycle arrest in G2/M phases. Conversely, forced expression of 14-3-3sigma showed the opposite effect. Furthermore, forced expression of 14-3-3sigma in human endometrial cell lines reduced cell growth and colony formation. CONCLUSIONS: We suggest that 14-3-3sigma in HECC suppresses cell proliferation and mediates DAC induced G2/M arrest and inhibition of cell proliferation in HECC.

AB - 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 14-3-3sigma on HECC oncogenicity in response to DAC treatment was evaluated in RL95-2 and AN3 cells after forced expression or silencing of 14-3-3sigma 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 14-3-3sigma. Silencing of 14-3-3sigma induced cellular proliferation and reduced the effect of DAC on cell cycle arrest in G2/M phases. Conversely, forced expression of 14-3-3sigma showed the opposite effect. Furthermore, forced expression of 14-3-3sigma in human endometrial cell lines reduced cell growth and colony formation. CONCLUSIONS: We suggest that 14-3-3sigma in HECC suppresses cell proliferation and mediates DAC induced G2/M arrest and inhibition of cell proliferation in HECC.

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