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Fig. 7 | Stem Cell Research & Therapy

Fig. 7

From: Elevated level of mitochondrial reactive oxygen species via fatty acid β-oxidation in cancer stem cells promotes cancer metastasis by inducing epithelial–mesenchymal transition

Fig. 7

Elevated mitochondrial ROS level promoted the epithelial mesenchymal transition via activation of MAPK signaling pathway. a RT-PCR analysis of redox-sensitive signaling pathways, including MEK1, MEK2, P38, and PI3K, and EMT related genes including PTGS2, MMP1, MMP2, LOX, ANGPTL4, CCL5, TWIST1, SNAI1, SNAI2, MET, ID1, and DARC in RH-TS cells and RL-TS cells. Results are shown as mean ± SEM from three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001. b Analysis of redox-sensitive signaling pathways and EMT related proteins. RH-TS cells had downregulation of an epithelial marker E-cadherin, and upregulation of mesenchymal markers vimentin and keratin-4. Redox-sensitive signaling pathways, including MEK1, MEK2, P38, and PI3K were significantly overexpressed in RH-TS compared to RL-TS cells. c Proposed mechanism of the mitochondrial ROS promoted cancer metastasis of RH-TS cells. Elevated ROS of tumor sphere activated the p38 MAPK signaling pathway and promoted EMT process thus enforced the metastases formation

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Stem Cell Research & Therapy

ISSN: 1757-6512