miR-200c regulates induction of apoptosis through CD95 by targeting FAP-1.

Molecular Cell
Robert SchickelMarcus E Peter

Abstract

Tumor progression shares many characteristics with the process of epithelial-to-mesenchymal transition (EMT). Cells that have undergone an EMT are known to have an increased resistance to apoptosis. CD95/Fas is an apoptosis-inducing receptor expressed on many tissues and tumor cells. During tumor progression CD95 is frequently downregulated, and tumor cells lose apoptosis sensitivity. miR-200 microRNAs repress both the EMT-inducing ZEB1 and ZEB2 transcription factors. We now demonstrate that miR-200c sensitizes cells to apoptosis mediated by CD95. We have identified the apoptosis inhibitor FAP-1 as a target for miR-200c. FAP-1 was demonstrated to be responsible for the reduced sensitivity to CD95-mediated apoptosis in cells with inhibited miR-200. The identification of FAP-1 as an miR-200c target provides a molecular mechanism to explain both the downregulation of CD95 expression and the reduction in sensitivity of cells to CD95-mediated apoptosis that is observed in the context of reduced miR-200 expression during tumor progression.

References

Jan 27, 2000·Cell·D Hanahan, R A Weinberg
Aug 5, 2000·International Journal of Cancer. Journal International Du Cancer·Y LiT Sato
Dec 6, 2000·European Journal of Biochemistry·Y NakaiT A Sato
Apr 6, 2001·The American Journal of Pathology·I Meinhold-HeerleinJ C Reed
Oct 13, 2001·BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology·P Savagner
Mar 26, 2003·Cell Death and Differentiation·M E Peter, P H Krammer
May 2, 2003·Molecular and Cellular Biology·Vladimir N IvanovZe'ev Ronai
Sep 25, 2003·Proceedings of the National Academy of Sciences of the United States of America·Alicia Algeciras-SchimnichMarcus E Peter
May 24, 2005·Biochimica Et Biophysica Acta·Marcus E PeterBryan C Barnhart
Feb 25, 2006·The EMBO Journal·Kyeong-Hee LeeAndrew C Chan
Aug 5, 2006·Journal of Cellular Biochemistry·Eva WieckowskiTheresa L Whiteside
May 8, 2007·Cell·Marcus E PeterDavid H Lynch
Jun 23, 2007·RNA·Nanna Rønbjerg ChristoffersenAnders H Lund
May 14, 2009·Molecular Cancer Therapeutics·Dawn R CochraneJennifer K Richer

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Citations

Nov 8, 2011·Breast Cancer Research and Treatment·Aglaya G IyevlevaEvgeny N Imyanitov
Feb 14, 2012·Journal of Mammary Gland Biology and Neoplasia·Aldema Sas-ChenYosef Yarden
Feb 22, 2012·Journal of Mammary Gland Biology and Neoplasia·Erin N HoweJennifer K Richer
Mar 19, 2013·Cancer Letters·Jeffrey T Chang, Sendurai A Mani
Sep 11, 2013·Nature Communications·Chad V PecotAnil K Sood
Nov 22, 2011·Nature Medicine·Bogdan MateescuFatima Mechta-Grigoriou
May 12, 2012·Nature Reviews. Cancer·Thomas Brabletz
Aug 18, 2012·Nature Reviews. Cancer·Heiko Hermeking
Oct 7, 2011·Experimental Diabetes Research·Lakshmi PulakatJames R Sowers
Nov 21, 2012·PloS One·Annika HauMarcus E Peter
Aug 27, 2013·International Journal of Molecular Sciences·Alessandra MagentaFabio Martelli
Jan 8, 2014·Theranostics·Thillai V SekarRamasamy Paulmurugan
Nov 23, 2013·Cancer Letters·Xiangling FengYaguang Xi
Dec 7, 2013·Cell Biochemistry and Biophysics·Haidong XuJianning Zhao
Apr 9, 2014·Journal of Huazhong University of Science and Technology. Medical Sciences = Hua Zhong Ke Ji Da Xue Xue Bao. Yi Xue Ying De Wen Ban = Huazhong Keji Daxue Xuebao. Yixue Yingdewen Ban·Bao-Ping ChangShi-Ying Yu
May 23, 2014·Apoptosis : an International Journal on Programmed Cell Death·Y ChenY Q Wei
Dec 31, 2014·Genetics Research International·Alessia CartaDuncan Ayers
Aug 20, 2011·Cancer Research·Sharanjot SainiRajvir Dahiya
Jan 14, 2012·Expert Opinion on Therapeutic Targets·María Villa-Morales, José Fernández-Piqueras
Dec 30, 2015·Journal of Clinical Medicine·Yohei ShimonoHironobu Minami
Jan 1, 2014·Journal of Cellular Biochemistry·Jianguo CuiJianming Cai
Jan 24, 2016·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Hao ZhanXiaowu Huang
Jun 8, 2012·Hepatobiliary & Pancreatic Diseases International : HBPD INT·Wei-Yun ChenHong Shu
Nov 22, 2011·Biochemical and Biophysical Research Communications·Yuxia ZhangLi Wang
Oct 12, 2011·Seminars in Cancer Biology·Stéphane AnsieauAlain Puisieux
Dec 15, 2010·European Journal of Cancer : Official Journal for European Organization for Research and Treatment of Cancer (EORTC) [and] European Association for Cancer Research (EACR)·Raquel T LimaM Helena Vasconcelos
Jul 22, 2014·International Journal of Cancer. Journal International Du Cancer·Quanquan SunLonghua Chen
Apr 29, 2015·Free Radical Biology & Medicine·Weiwei LiHongying Wang
Mar 14, 2013·Cell Biology International·Zhi-Gang CaiXiao-Ping Xu
Sep 20, 2012·Journal of Cellular Biochemistry·Jing LinJianming Cai
Aug 14, 2010·EMBO Reports·Simone Brabletz, Thomas Brabletz

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