Research Paper Volume 12, Issue 13 pp 12771—12782
HOTAIR expands the population of prostatic cancer stem-like cells and causes Docetaxel resistance via activating STAT3 signaling
Figure 2. STAT3 activation is indispensable for the contribution of HOTAIR to cancer stemness. (A) Western blotting revealed that HOTAIR overexpression enhanced the expression levels of Sox2, Nanog and Oct4. GAPDH was used as internal control. (B) HOTAIR activated STAT3 signaling in both C4-2 cells and Du145 cells, monitored by p-STAT3 (Y705). GAPDH was internal control. (C, D) STAT3 inhibitor, S3I-201 (10 μM), could interrupt HOTAIR induced PCSLCs population in both C4-2 cells (C) and Du145 cells (D). Left, representative images of tumorspheres. Right, statistical analysis. *p<0.05; **p<0.01.