Fig 2: BAF53a expression is upregulated in glioma. (A) The representative images of BAF53a expression is detected by IHC in glioma tissues (scored as - to +++). Magnification, ×400. (B) The real-time PCR results show that the expression level of BAF53a mRNA in glioma tissues was higher than that in normal brain tissues. The expression profile of BAF53a in Oncomine database: BAF53a gene copy number in astrocytoma is higher than normal brain tissues in Sun brain data (C), and BAF53a gene copy number in glioblastomas is significantly higher than normal brain tissues in TCGA brain data and Murat brain data (D). *P<0.05; **P<0.01.

Fig 3: BAF53a associates with EMT in glioma. The expression correlation of BAF53a, vimentin and E-cadherin in glioma cells detected by real-time PCR (A) and western blotting (B), results showed that vimentin expression was upregulated along with BAF53a overexpression, but E-cadherin expression was decreased; when BAF53a was knocked down, they had inverse expression. (C) The phase contrast images of BAF53a-interfered U87 cells, results showed cells became mesenchymal-like in BAF53a overexpression, and cells changed to oval or cobblestone-like appearance in BAF53a knockdown. (D) The representative images of expression correlation of BAF53a, vimentin and E-cadherin in glioma tissues detected by IHC. (E) The Spearman's rank correlation test indicated that BAF53a and vimentin expression were positively correlated, while BAF53a and E-cadherin expression were negatively correlated.

Fig 4: ACTL6A is required for FSH-induced ovarian cancer cell glycolysis.a, b Treatment with FSH upregulates ACTL6A expression in a dose- (a) and time-dependent (b) manner in HO8910 and OVCAR-3 cells. c Knockdown of FSHR blocks FSH-enhanced ACTL6A expression. d–f Glucose uptake (d), lactate production (e), and pyruvate level (f) were measured in HO8910 and OVCAR-3 cells stimulated by FSH with or without shACTL6A as indicated. *p < 0.01. g Knockdown of ACLT6A eliminates FSH-induced PGK1 expression

Fig 5: FSH upregulation of ACTL6A and PGK1 depends on PI3K/AKT signaling.a Genetic profiling of ACTL6A and PIK3CA co-occur in ovarian cancer from TCGA databases determined by cBioPortal analysis (http://www.cbioportal.org/). b Scatterplots of ACTL6A mRNA expression vs. PIK3CA copy number in ovarian cancer from TCGA databases. c LY294002 blocks FSH-induced ACTL6A and PGK1 expression and AKT activation. d–f Glucose uptake (d), lactate production (e), and pyruvate level (f) were measured in HO8910 and OVCAR-3 cells stimulated by FSH with or without LY294002 as indicated. *p < 0.01