Skip to main content
. 2014 Sep 9;5(19):9514–9529. doi: 10.18632/oncotarget.2413

Figure 6. FOXF1 mediates reprogramming effects on fusion progeny.

Figure 6

(A) FOXF1 mRNA levels were determined by real-time PCR in fusion progeny and parent cell lines. Values (means + SEM) are normalized to eEF1α and the H441 level = 1.0; *, P<0.05; **, P<0.01; ***, P<0.001 using paired t-tests. (B) Western blots of and EMT proteins in fusion progeny #12 transfected with shFOXF1 or shControl; actin served as loading control. (C) Knockdown of FOXF1 reduces MSC-specific cell surface marker expression in fusion progeny #12. Average (+ SEM) fold changes of indicated surface markers in fusion progeny #12 transfected with shFOXF1 and shControl; *** indicates P<0.001 in unpaired t-tests with Welch's correction, compared to isotype control. (D) Down-regulation of FOXF1 in fusion progeny #12 increases cell growth. Values are means ± SEM; *** indicates P<0.001 using two-way ANOVA. (E) Western blots of cell cycle regulatory proteins in fusion progeny #12 transfected with shFOXF1 or shControl; actin served as loading control. (F) A schematic showing that FOXF1 mediates MSC fusion-induced reprogramming of lung cancer cells via regulating cell cycle- and EMT-pathways leading to non-tumorigenic, stem-like state of fusion progeny.