https://www.selleckchem.com/pr....oducts/Sunitinib-Mal
Additionally, pc-Jun and phosphorylated JNK were localized in the nuclear in addition to displaying enhanced expression in the EC tissues. IRS2 overexpression negated the inhibition of cell proliferation, invasion and sphere formation triggering YAP silencing. YAP up-regulated IRS2 and aggravated EC in vivo. Taken together, YAP-TEAD activates the JNK/c-Jun pathway to up-regulate IRS2, ultimately promoting EC progression. Therefore, YAP-TEAD inhibition could be a promising therapeutic approach for EC treatment.Parentifi
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