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- W2968909110 abstract "LB-44 Autophagy usually occurs in response to nutrient depletion or growth factor withdrawal. Glycogen synthase kinase 3 (GSK-3) is a protein serine/threonine kinase involved in multiple cellular functions, and its activity in cells increases dramatically under the condition of serum starvation. Because serum starvation leads to autophagic response in cells, we sought to understand if GSK-3 controls autophagic activities after serum depletion. Consistent with previous reports, serum starvation led to autophagic responses including LC-3 processing and MDA-positive staining in rostate cancer PC-3 and LNCaP cells. Treatment of serum-starved cells with GSK-3 inhibitors, peptide inhibitor L803mts but not PI3K inhibitor LY294002, caused a profound necrostic cell death. L803mts-induced cell death could not be suppressed by a broad caspase inhibitor and no caspase activation and PARP cleavage (apoptotic features) were detected indicating an non-apopotic cell death. However, autophagy suppressor 3-methyladenine (3-MA) did not block L803mts-induced cell death but shift the necrotic cell death response to a dramatic apoptotic response, as evidenced by caspase activation and PARP cleavage. No significant cell death was observed under full culture media (10% serum) with the GSK-3 inhibitor L803 or 3-MA. Taken together, our data suggest that GSk-3 activity is critical for autophagy-dependent survival under the condition of serum starvation, and suppression of autophagy converts GSK-3 inhibition-induced necrotic cell death to apoptotic cell death. This study opened a novel field regarding GSK-3’s control of cell survival." @default.
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- W2968909110 date "2008-05-01" @default.
- W2968909110 modified "2023-09-22" @default.
- W2968909110 title "GSK-3 modulates autophagy after growth factor depletion" @default.
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