Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 231 - 240 |
| Number of pages | 10 |
| Journal | Gynecologic Oncology |
| Volume | 127 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2012 |
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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 journal › Article › Research › peer-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.
UR - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=22772061
U2 - 10.1016/j.ygyno.2012.06.039
DO - 10.1016/j.ygyno.2012.06.039
M3 - Article
VL - 127
SP - 231
EP - 240
JO - Gynecologic Oncology
JF - Gynecologic Oncology
SN - 0090-8258
IS - 1
ER -