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. 2020 Jul 13;12(13):12771–12782. doi: 10.18632/aging.103188

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Copyright © 2020 Wang et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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HOTAIR contributes to Docetaxel resistance of PCa cells. (A, B) overexpression of HOTAIR caused Doc resistance in C4-2 (A) and Du145 cells (B). (C) Top, carton showed how C4-2 DocR cells were established. Bottom, C4-2 DocR cells expressed higher levels of HOTAIR and cancer stem cells markers. Gene expression was normalized to GAPDH mRNA. (D) Cancer stem cells markers (Sox2, Nanog and Oct4) were overexpressed in C4-2 DocR cells compared to parental cells. GAPDH was internal control. (E) left, knockdown of HOTAIR restore Doc sensitivity of C4-2 DocR cells; right, knockdown efficiency of HOTAIR in C4-2 DocR cells. (F) knockdown of HOTAIR impaired the tumor sphere forming ability of C4-2 DocR cells. Left, representative images of tumorspheres. Right, statistical analysis. p<0.05; **p<0.01.