Fig. 6: p-STAT5 interacts with SREBP1 and promotes its transcriptional activity. | Cell Death & Disease

Fig. 6: p-STAT5 interacts with SREBP1 and promotes its transcriptional activity.

From: mTOR direct crosstalk with STAT5 promotes de novo lipid synthesis and induces hepatocellular carcinoma

Fig. 6

a Related hepatic mRNA (qPCR) from 10-month-old L-TKO and control mice (left, n = 5, ***P < 0.001), and p-STAT5-plasmid treated HepG2 cells (right, n = 6, ***P < 0.001). b Relative luciferase activity was detected after HepG2 cells were co-transfected with SREBP1 promoter and p-STAT5-siRNA or p-STAT5-plasmid (n = 6, ***P < 0.001). c Liver tissues were collected and stained with anti-SREBP1 showed significantly accumulated both in the cytoplasm and the nuclear componets in L-TKO mice (n = 4, ***P < 0.001). d HepG2 cells were treated with p-STAT5-siRNA or p-STAT5-plasmid to downregulate or upregulate p-STAT5, which affected the nuclear distribution of SREBP1 (n = 6, ***P < 0.001). e HepG2 cells were treated with siRNA or inhibitor IN-1 to downregulate p-STAT5, which reduced the expression of SREBP1 (m), ACC1 and FASN. Western blots were quantified. n = 4, ***P < 0.001. HepG2 cells were treated with inhibitor IN-1(f) or siRNA (g) to inhibit p-STAT5 in advance, which decreased lipid accumulation induced by oleic acid and palmitic acid, confirmed by BODIPY493/503 staining

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