Fig 1: Target relationship between miR-107 and RGS4 detected by dual-luciferase reporter gene assay. The target scan database revealed that RGS4 may be a potential target gene of miR-107; dual-luciferase reporter assays detected that miR-107 targets RGS4. Values are expressed as the mean ± standard deviation of three independent experiments. **P<0.01 vs. 3′-UTR-MUT. miR, microRNA; RGS4, regulator of G-protein signaling 4; 3′-UTR, 3′-untranslated region; WT, wild-type; MUT, mutant.
Fig 2: Protein expression levels of RGS4, EGFR, CXCR4 and MMP-2 and −9. (A) Western blot analysis and (B) quantification. **P<0.01 vs. NC and control mimics. NC, negative control; RGS4, regulator of G-protein signaling 4; EGFR, epidermal growth factor receptor; CXCR4, CXC chemokine receptor 4; MMP, matrix metalloproteinase; miR, microRNA; NC, negative control.
Fig 3: RGS5 is the key downstream of ATE1 to regulate the deregulation of β-catenin. A, The expressions of ATE1 and its downstream proteins RGS4, RGS5, RGS16 were detected by indicated antibodies. B, Representative IHC images of RGS5 and β-catenin expression in HCC serial slices. Magnification, 100×; inset magnification, 400×. The correlation analysis between RGS5 and β-catenin was shown in the table below. C, The expression of ATE1 was determined by real-time PCR and Western blot analysis, respectively in RGS5-intervened HepG2-shATE1 and HCCLM3-ATE1 cell lines. D, The expression of β-catenin and its representative downstream proteins were monitored in with or without RGS5 intervening cell lines by Western blot analysis using the indicated antibodies. E, HCC cells were treated with cycloheximide at different time points as indicated followed by Western blot analysis using the indicated antibodies.
Fig 4: The Potential Mechanism of BUB1B in BC. A-B Western blot analysis of the protein related to the chemokine binding and inflammatory response (CDC25A, IFI6, CXCR6, RGS4) and BUB1B levels. C NF-κ B signaling pathway was enrichment via GSEA analysis in BUB1B-overexpressing bladder cancer cells. D Western blotting showed the expression of p65, P-p65, IκBα and P-IκBα in NF-κB pathway in BUB1B-overexpressing UMUC-3 bladder cancer cells. E Western blotting was performed to test the expression of BUB1B, p65, P-p65, CXCR6 and IFI6 in BUB1B-overexpressing UMUC-3 cells treated with or without NF-κB inhibitor PDTC 10 μm for 48 h. F Invasion assay conducted on BUB1B-overexpressing UMUC-3 cells in the presence or absence of NF-κB inhibitor PDTC. (* p < 0.05, ** p < 0.01)
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