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Results: The ShRNA directed against GPR34 effectively inhibited both endogenous mRNA and protein expression levels of GPR34, and significantly down-regulated the expression of PIK3CB (P < 0.
Among the intracellular components in the insulin-signaling pathway, IGF2 expression was the most abundant, followed by AKT1, IGF2R, INSR, IRS1 and IGF1R, but the mRNA levels of INS1, INS2, PIK3CB, and SHC1 were very low in the adipocytes.
PIK3CA and PIK3CB inhibition produce synthetic lethality when combined with estrogen deprivation in estrogen receptor-positive breast cancer.