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. Author manuscript; available in PMC: 2016 Aug 10.
Published in final edited form as: Oncogene. 2015 Dec 7;35(29):3781–3795. doi: 10.1038/onc.2015.444

Figure 4. HMGA2 regulates stemness and epithelial-mesenchymal plasticity in prostate tumor cells with PI3K/AKT and RAS/MAPK co-activation.

Figure 4

(a) ShRNA-targeted knockdown of HMGA2 protein expression in PKV cells. Mouse embryonic stem cells (M. ESC) were used as a positive control for HMGA2 expression. β-actin was used as a loading control. Control, PKV cells. Scramble, shScramble. (b) The proliferation of the PKV-shScramble (Scramble) and PKV-shHmga2 (shHmga2) cell lines was measured by MTT assay and is presented as % growth compared to control PKV cells. (c) PKV cells stably expressing shHmga2 have significantly reduced matrigel sphere-forming capacity compared to control PKV-shScramble (Scramble) cells. (d) HMGA2 knockdown reduces the expression of a number pluripotency and self-renewal factors. Expression is relative to gene expression values found in PKV-shScramble (Scramble) cells. (e) FACS analysis of the PKV-shScramble (Scramble) and PKV-shHmga2 cell lines revealed that throughout passaging, PKV-shHmga2 cells maintained a lower percentage of MES-like and higher percentage of EMT tumor cells compared to PKV-shScramble cells, indicative of a blockade in the transition of EMT tumor cells into fully MES-like tumor cells. (f) FACS sorted MES-like tumor cell populations from PKV-shHmga2 cells have reduced mesenchymal content and increased epithelial and EMT tumor cell numbers compared to control PKV-shScramble (Scramble) cells after 7 days in culture. Data in b-f are represented as mean ± SEM from 2-3 independent experiments done in triplicate. *, p<0.05; **, p<0.01.