Fig 1: CD24-induced signaling routes for cellular quiescence-like state and chemoresistance in ovarian cancer cells.CDK19 plays a role in cell proliferation in ovarian cancer by being expressed in the absence of CD24 signaling. However, in the presence of CD24 signaling, miR-130a and 301a are expressed through Src-mediated STAT4 activation and Src and FAK-mediated YY1 activation. This results in the degradation of CDK19 mRNA, causing ovarian cancer cells to enter a quiescence-like state and become resistant to chemotherapy.
Fig 2: STAT4 and YY1-mediated regulation of miR-130a and 301a expression in CD24-high ovarian cancer cells.A Putative binding site for STAT4 and YY1 on MIR130A and MIR301A promoter regions. ※ s: site. B Chromatin immunoprecipitation of MIR130A and MIR301A promoter using anti-STAT4 and YY1 antibodies. ※ S: segment. Real-time PCR analysis of C STAT4 or YY1-dependent and D Src or FAK-mediated miR-130a, 301a, and CDK19 expression in CD24-high ovarian cancer cells. Western blot analysis of E STAT4-dependent, F YY1-dependent, and G Src or FAK-mediated CDK19 expression in CD24-high ovarian cancer cells.
Fig 3: RNA synthesis regulation by CD24-miR-130a/301a-CDK19 signaling axis in ovarian cancer cells.A Functional annotation analysis of the putative target genes of miR-130a and 301a. B Analysis of CD24, miR-130a, miR-301a, or CDK19 expression-dependent RNA synthesis. Representative images (left). The graphs with all images’ integrated relative density values (right).
Fig 4: Expression of the CD24-miR-130a/301a-CDK19 signaling axis components in patient tissues and their relation with patient survival.A CD24-dependent expression of miR-130a, miR-301a, and CDK19 in ovarian cancer patient tissues. a Venn diagram presentation of sub-type distribution in the ovarian cancer patient tissue pool. The patient tissues were grouped into CD24-high and low. b Expression comparison analysis of miR-130a, miR-301a, and CDK19 between CD24-low and high ovarian cancer patient tissues. B Survival comparison analysis between ovarian cancer patient groups with low and high expression of CD24, CDK19, miR-130a, and miR-301a. Survival graphs were plotted using the KM plotter.
Fig 5: CSC-like phenotype manifestation by miR-130a and 301a-dependent CDK19 downregulation in ovarian cancer cells.A Binding assay of miR-130a and 301a to CDK19 3’UTR. B Real-time PCR analysis and C Western blot analysis of CDK19 expression in miR-130a or 301a expression-manipulated ovarian cancer cells. Analyses for D cell cycle, E Colony forming ability, F Cell proliferation, and G IC50 in CDK19-expression-manipulated ovarian cancer cells. H Expression analysis of CDK19 transcript in miR-130a/301a-low and high ovarian cancer clones. All the clones were derived from the same ovarian cancer patient.
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