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. 2016 Mar 10;7(3):e2137. doi: 10.1038/cddis.2016.41

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Copyright © 2016 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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CASP2 serves as an initiator in HOTAIR knockdown induced apoptosis. (a) Upregulation of full-length CASP2 and cleavage of CASP2 and CASP3 was detected after HOTAIR knockdown. (b) Overexpressed CASP2 cleaved itself and activated CASP7. (c) Overexpression of CASP2 induced apoptosis in HCT116 cells. (d) pcDNA3.1(-)-CASP2 aggravated activation of CASP3 and siCasp2 reduced that. (e) SiCasp2 rescued the apoptosis caused by siHOT1. (f) MiR-125a-5p diminished cleavage of CASP2 and CASP7 and inhibition of miR-125a-5p aggravated that. Bars represent the mean±S.E.M. from three independent experiments. *P<0.05, ***P<0.001 by Student's t-test. All experiments were performed in three biological repeats