XIST regulated miR-29c by directly targetting in TMZ-resistant glioma cells XIST regulated miR-29c by directly targetting in TMZ-resistant glioma cells.

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XIST regulated miR-29c by directly targetting in TMZ-resistant glioma cells XIST regulated miR-29c by directly targetting in TMZ-resistant glioma cells (A) LN229/TMZ and U251/TMZ cells were transfected with mimics NC/miR-29c mimics or inhibitor NC/miR-29c inhibitor. Expression of miR-29c was verified using real-time PCR assays. (B) LN229/TMZ and U251/TMZ cells were transfected with mimics NC/miR-29c mimics or inhibitor NC/miR-29c inhibitor. Expression of XIST in response to miR-29c overexpression or inhibition was determined using real-time PCR assays. (C) LN229/TMZ and U251/TMZ cells were transfected with siRNA-NC/siRNA-XIST. Expression of miR-29c in response to XIST knockdown was determined using real-time PCR assays. (D,E) Association of miR-29c and XIST with AGO2 in LN229/TMZ and U251/TMZ cells. Detection of AGO2 and IgG using Western blotting (D). Detection of miR-29c and XIST using real-time PCR (E). (F) wt-XIST and mut-XIST luciferase reporter gene vectors were constructed by mutating the putative binding site of miR-29c in XIST. (G) The indicated vectors were cotransfected into the TMZ-resistant glioma cells (U251/TMZ) with miR-29c mimics or miR-29c inhibitor. The luciferase activity in each group was then determined using dual luciferase assays. The data are presented as mean ± S.D. of three independent experiments; **P<0.01. Peng Du et al. Biosci. Rep. 2017;37:BSR20170696 ©2017 by Portland Press Ltd