https://www.selleckchem.com/products/ars-1323.html
Overexpression of UBE2T promoted proliferation, migration, invasion and glycolysis in BCa cells, while UBE2T knockdown showed the opposite results. Moreover, UBE2T knockdown suppressed tumor growth in mice. Further mechanism analysis shows that UBE2T participated in the regulation of BCa progression through affecting the PI3K/AKT signaling pathway. UBE2T promoted proliferation, invasion and glycolysis through modulating PI3K/AKT signaling pathway in BCa, implying that UBE2T may provide a promising therapeutic target for the therapy of
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