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Fig. 6 | Cancer Cell International

Fig. 6

From: miR-320a/SP1 negative reciprocal interaction contributes to cell growth and invasion in colorectal cancer

Fig. 6

miR-320a modulated the oncogenic MACC1/MET signaling pathway through SP1. Previous study identified SP1-binding elements within the MACC1 promoter region. We performed a luciferase reporter assay to confirm whether SP1 modulates MACC1 transcriptionally. a A schematic diagram showing the previously identified SP1 binding site (− 172 to − 166) and a predicted one (− 445 to − 436) within 500 bp upstream of the MACC1 TSS. (B) SP1 enhanced luciferase activity by recognizing the wild-type MACC1 promoter, and the enhancement was abrogated by its mutated counterpart. (P < 0.0001). c Immunoblotting assays showed that ectopic miR-320a expression apparently inhibited SP1 expression followed by MACC1 inhibition. As downstream effectors of MACC1, c-MET, p-ERK1/2, and p-AKT were repressed along with ectopic miR-320a expression. Normalized intensity of each immunoblot was analyzed and is annotated below the stripes. d Decreased mRNA expression of SP1 and MACC1 induced by miR-320a was also observed in xenograft mouse tumor tissues. SP1: SP1 expressing vector; Ctrl: control vector; pMACC1-wt: wild-type promoter sequence of MACC1 (− 500 to + 1 bp) subcloned into a pGL4.10 luciferase reporter vector; pMACC1-mut: mutant counterpart of MACC1 promoter sequence created by deletion mutation of the two mentioned SP1 binding elements

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