Research Paper Volume 14, Issue 5 pp 2268—2286

A comprehensive analysis of FOX family in HCC and experimental evidence to support the oncogenic role of FOXH1

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Figure 5. FOXH1 mediated cell growth and cell migration/cell invasion of HCC cells were dependent of mTOR signaling. (A) GSEA KEGG analysis showed that mTOR signaling was enriched in high FOXH1 HCC patients. (B) FOXH1 mediated cell growth of HA22T and SK-HEP-1 cells was blocked by mTOR inhibitor rapamycin (Rapa). (C) Colony formation assay showed that FOXH1 induced cell growth of HA22T cells was attenuated by rapamycin. Left, representative images of colonies. Right, statistical analysis. (D) FOXH1 lost the ability to increase cell migration of HA22T and SK-HEP-1 cells in the presence of rapamycin. Top, representative images of wounding healing assay. Bottom, statistical analysis. (E) FOXH1 failed to increase cell invasion of HA22T and SK-HEP-1 cells in the presence of rapamycin. Top, representative images of invading cells. Bottom, statistical analysis. (F) FOXH1 induced phosphorylation levels of S6K1 were blocked by rapamycin. GAPDH served as loading control. *P<0.05, **P<0.01, ***P<0.001.