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. 2021 Dec 6;7:376. doi: 10.1038/s41420-021-00771-y

Fig. 6. STAT1, an oncogene of BC, was directly regulated by miR-512-5p.

Fig. 6

a Putative binding sites between miR-512-5p and STAT1 3′-UTR were predicted. Plasmids containing WT (up) or MUT (down) sequences of the putative binding sites were constructed. b Dual-luciferase reporter assay was performed to detect the binding between miR-512-5p and STAT1 3′-UTR. c The transcription level of STAT1 in BC cells transfected with miR-NC or miR-512-5p inhibitor was detected by RT-qPCR. d–e The protein levels of STAT1 in miR-NC group and miR-512-5p inhibitor group were analyzed by western blotting. ACTIN was employed as internal control. f The mRNA level of STAT1 was detected by RT-qPCR after overexpression of miR-512-5p. g–h The protein levels of STAT1 in miR-NC group and miR-512-5p mimics group were analyzed by western blotting. ACTIN was used as internal control. i Efficiency of si-STAT1 was determined by RT-qPCR. j–k MTT assay was conducted to explore the proliferation of MDA-MB-231 (j) and MCF-7 (k) cells when STAT1 was inhibited by si-STAT1. l–m Colony formation assay was performed to compare the colony formation ability of si-NC group and si-STAT1 group (l). Colony numbers were counted (m). n–o The migration of MDA-MB-231 cells transfected with si-NC or si-STAT1 was analyzed by wound-healing assay. Photographs were taken at 0 and 24 h after scratching (n). Wound closure was analyzed (o). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.