https://www.selleckchem.com/products/pr-619.html
In addition, the in vivo experiments illustrated that the up-regulation of FAST1 strengthened tumor growth. On the contrary, knocking down FAST1 had the opposite effects. Mechanistically, The TGF-β/Smad pathway contributed to RC evolvement and was activated by FAST1 both in vitro and in vivo. This article suggests that FAST1 exerts a carcinogenic role in RC by regulating the TGF-β/Smad signaling. This article suggests that FAST1 exerts a carcinogenic role in RC by regulating the TGF-β/Smad signaling. To explore the molecular mechanism of
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