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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

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

Fig. 6

The RGCC/PLK1 axis activates AMPKα2. A The significant pathways associated with PLK1 were enriched by SangerBox based on the PLK1 potential phosphorylated proteins. B Determination of AMPKα2 phosphorylation in vitro. The experiments were independently repeated three times, with the error bars denoting the S.D. C Western blots of p-AMPK and p-ACC proteins in RGCC knockdown or overexpression tumor cells. D Orthotopic metastasis of RGCC overexpressed MDA-MB-468 cells treated with or without PLK1 inhibitor (Volasertb) or AMPK inhibitor (Dorsomorphin). Volasertib at 25 mg/kg, dorsomorphin at 0.2 mg/kg, or O304 at 200 mg/kg were given twice per week by oral gavage after the mouse’s tumor volume was above 50 mm3. Representative pulmonary surface nodules (n = 7 mice per group) are shown. E Immunostaining of p-AMPKα2 (T172) in lung metastatic tissues of mice with different treatments. F p-AMPKα2 (T172) protein levels in lung metastatic tissues of mice with different treatments were determined by western blotting

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