Fig 2: Model for Proposed Role for ACTL6A in ovarian cancer.The schematic describes a proposed model for the role of ACTL6A involved in FSH-driven glycolysis in ovarian cancer cells through upregulating PGK1

Fig 3: 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

Fig 4: Expression pattern of ACTL6A in cervical cancer. (A) Genetic and expression alteration of the subunits of SWI/SNF complex in 310 samples of CESE available at TCGA database by using cBioPortal. (B) mRNA expression levels of ACTL6A in various types of cancer from Oncomine. The red or blue intensity is directly proportional to the significance expression level of upregulation or downregulation, respectively. (C) Analysis of ACTL6A expression in normal cervix, cervical intra-epithelial neoplasia (CIN) and cervical cancer in GSE63514. (D–F) Analysis of ACTL6A expression in normal cervix and cervical cancer in GSE7803, GSE6791 and GSE9750. Error bar = mean ± SD, *p < 0.01.

Fig 5: Identification of biological processes and signaling pathways. (A) Gene set enrichment analysis showed the correlation between ACTL6A and KEGG pathway in cervical cancer available at LinkedOmics. (B) GSEA enrichment plots showed that a series of gene sets including REACTOME CELL CYCLE, REGULATION OF CELL CYCLE, WHITFIELD CELL CYCLE LITERATURE and MITOTIC CELL CYCLE were enriched in the ACTL6A-high group. NES, normalized enrichment score; FDR, false discovery rate.