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Fig. 5 | Molecular Medicine

Fig. 5

From: HNRNPC promotes collagen fiber alignment and immune evasion in breast cancer via activation of the VIRMA-mediated TFAP2A/DDR1 axis

Fig. 5

VIRMA and HNRNPC participate in the m6A regulation of TFAP2A. Note: (A) Cuilab database predicted the m6A sites on TFAP2A mRNA, and the abscissa represents the location of the m6A sites on mRNA, and the ordinate represents the prediction score of the m6A sites, and the higher the score, the greater the possibility of m6A modification at the site; (B) Correlation analysis of TFAP2A and m6A regulatory factors HNRNPA2B1, HNRNPC, VIRMA, and WTAP in breast cancer-related TCGA dataset, including 1096 breast cancer tissues; (C) RT-qPCR detected the expression levels of HNRNPA2B1, HNRNPC, VIRMA, and WTAP in breast cancer cells (EO771, EMT6, and 4T1.2); (D) Schematic diagram of m6A regulatory mechanism; (E) RT-qPCR and Western blot detected the expression levels of VIRMA and HNRNPC in each group of EO771 cells after silencing; (F) RT-qPCR detected the expression levels of TFAP2A in each group of EO771 cells after silencing of VIRMA and HNRNPC; (G) RT-qPCR detected the expression levels of VIRMA, HNRNPC, and TFAP2A in each group of EO771 cells; (H) Me-RIP detected the m6A methylation level of TFAP2A mRNA in each group of EO771 cells; (I) PAR-CLIP experiment detected the binding of VIRMA to TFAP2A mRNA in each group of EO771 cells; (J) RIP experiment detected the m6A modification recognition of TFAP2A mRNA by HNRNPC in EO771 cells. * indicates P < 0.05, ** indicates P < 0.01 compared with the control group. All cell experiments were repeated 3 times

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