https://www.selleckchem.com/products/indy.html
Correlations between the expressions of TMEM245 and miR-32, FOXK1 and miR-32, and FOXK1 and TMEM245 were positive and significant. FOXK1-knockdown led to decreased miR-32 and TMEM245 expression and increased PTEN expression, whereas FOXK1-overexpression had the opposite effect. Overexpressed FOXK1 promoted the malignancy of CRC cells in vitro by stimulating proliferation and reducing apoptosis; whereas FOXK1-depletion suppressed such malignancy and a miR-32 inhibitor partially reversed the effects of FOXK1. The results of ChIP and dual-luc
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