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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: The RNA-binding protein GRSF1 promotes hepatocarcinogenesis via competitively binding to YY1 mRNA with miR-30e-5p

Fig. 3

YY1 is an essential target of GRSF1, and feedback promoted GRSF1 expression. A GRSF1 and YY1 expression in HCC cells cotransfected with sh-GRSF1 and ov-YY1 vectors. B-E YY1 overexpression rescued the tumor-inhibiting effect caused by GRSF1 knockdown on HCC cell proliferation (B), cell apoptosis (C), colony formation (D) and migration (E) ability. The invaded cells in Transwell assays were quantified by counting the cells in 10 random fields (magnification, 200×). F GRSF1 expression levels in HCC cells were decreased following inhibition of YY1. G GRSF1 expression in HCC cells was increased following overexpression of YY1. H ChIP analysis of YY1-HA tagged fusion vector levels at the GRSF1 promoter in MHCC-97H and Hep3B cells. ChIP results were analyzed via qRT–PCR using GRSF1 promoter-specific primers and are expressed as the percentage of the input. Rpb1 was used as a positive control for GRSF1 ChIP. IgG was used as a negative control. Values are the mean± SEM (= 3). *< 0.05, **< 0.01

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