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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: RGCC-mediated PLK1 activity drives breast cancer lung metastasis by phosphorylating AMPKα2 to activate oxidative phosphorylation and fatty acid oxidation

Fig. 7

RGCC/PLK1/AMPKα2 signaling takes a role in TNBC lung metastasis. A Volcano plots of metabolites in RGCC knockdown MDA-MB-231/LM3 vs MDA-MB-231/LM3 control cells. B The enriched metabolic signaling pathways based on the genes regulating the high changed metabolites in control MDA-MB-231/LM3 cells. C Mitochondrial membrane potential was determined by JC-1 staining. D Oxygen consumption rate (OCR) was measured using a Seahorse XF24 Extracellular Flux Analyzer. E Fatty acid oxidation was detected using microplate reader. F ROS levels were measured by DCFH-DA probe. G Orthotopic metastasis of RGCC knockdown MDA-MB-231/LM3 cells was assessed in mice under treated with or without OXPHOS inhibitor (IACS-10759) or fatty acid oxidation inhibitor (Etomoxir). IACS-10759 at 25 mg/kg or Etomoxir at 20 mg/kg was given orally for 5 days followed by 2 days off every week, when the mice's tumor growth reached about 50 mm3. Representative pulmonary surface nodules (n = 7 mice per group) were shown. (Data are means ± SD from 3 independent experiments; ***P < 0.001)

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