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. Author manuscript; available in PMC: 2010 Dec 8.
Published in final edited form as: Cancer Cell. 2009 Dec 8;16(6):498–509. doi: 10.1016/j.ccr.2009.10.014

Figure 7. MET oncogene regulates miR-221&222 activation.

Figure 7

(A-B-C) Relative expression levels of miR-221&222 in Calu-1, Snu-387 and GTL16 after transfection with miR control and siRNA MET. MiR-221&222 expression decreased after MET knockdown. (D-E-F) Western blots after siRNA MET transfection in Calu-1, Snu-387 and GTL16 cells. MET knockdown decreased miR-221&222 expression levels, giving rise to PTEN and TIMP3 upregulation in all the different cell lines. GTL16 cells were moreover treated for 24h with 4μM of the MET inhibitor SU11274. MET inhibition increased miR-221&222 targets expression levels. (G-H-I) Identification of c-Jun (AP-1) interacting region by using 2 different amplicons across the miR-221/222 transcription start site. ChIP analysis was performed with chromatin from H460 c-Jun negative cells, Calu-1 and Snu-387 c-Jun positive cells. BS=binding site. (L) qRT-PCR of miR-221&222 in Huh7 cells after treatment with anisomycin (10 μM) for 30’. Anisomycin induced miR-221&222 upregulation. (M) Anisomycin induced c-Jun activation and PTEN and TIMP3 downregulation in Huh7 cells. Total lysate was analyzed by western blot using anti-PTEN and anti-TIMP3 antibody. Error bars indicate ±SD.