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. 2023 Jun 13;9(6):e16865. doi: 10.1016/j.heliyon.2023.e16865

Fig. 7.

Fig. 7

Molecular mechanism of DSCAS mediating cisplatin sensitivity. (A). Bioinformatics analysis showed that DSCAS, mRNA of Bcl-2 and Survivin have targeted binding sites to miR-646-3p. (B–D). The expressions of miR-646-3p, Survivin and Bcl-2 mRNA in cancer tissues and adjacent normal tissues were compared using RT-qPCR assay. (n = 63, P < .05). (E). DSCAS was negatively correlated with miR-646-3p in tissues. (n = 63, R2 = 0.49, P < .05). (F–G). DSCAS were positively correlated with Survivin and Bcl-2 mRNA. (n = 63, R2 = 0.50,0.47, respectively, all P < .05). (H–J). Dual luciferase reporter gene assay confirmed DSCAS, mRNA of Bcl-2 and Survivin could bind to miR-646-3p. (K–N). RNA-IP and RNA Pull-down assay confirmed DSCAS, mRNA of Bcl-2 and Survivin could bind to miR-646-3p. (O). The expression of miR-646-3p was assessed using RT-qPCR assay in stably transfected SK-MES-1 cell lines harboring sh-DSCAS, sh-NC, oe-DSCAS or oe-NC, respectively. (n = 3, P < .05). (P). MiR-646-3p was overexpressed in SK-MES-1 cells via Lipofectamine 3000 transient transfection and verified by RT-qPCR. (n = 3, P < .05). (Q). The relative expression of Bcl-2 and Survivin were detected using Western blotting assay. (R). Histogram displayed relative expression of Bcl-2 and Survivin. (n = 3, P < .05). *P < .05,**P < .01,***P < .001，****P < .0001 compared with control.