https://www.selleckchem.com/products/Daidzein.html
Specifically, TET2 offsets the elevation of p-AKT level induced by FGFR3∆7-9 through directly binding to PTEN promoter and increasing 5-hmC. Therefore, through phosphorylation and inhibition of TET2, FGFR3∆7-9 reduces PTEN expression and substantiates AKT activation to stimulate HCC proliferation. Together, this study identifies TET2 as a key regulator of the oncogenic role of FGFR3∆7-9 in HCC carcinogenesis and sheds light on new therapeutic strategies for HCC treatment.Inactivation of tumor suppressor gene played critical roles in th
Like
Comment
Share
