ArticleMolecular and cellular biochemistry2018
GDC-0152-induced autophagy promotes apoptosis in HL-60 cells.
Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Dual role of endoplasmic reticulum stress-ATF-6 activation in autophagy and apoptosis induced by cyclic stretch in myoblast.Apoptosis : an international journal on programmed cell death · 2023Article
- SMAC Mimetic BV6 Co-Treatment Downregulates the Factors Involved in Resistance and Relapse of Cancer: IAPs and Autophagy.Biology · 2022Article
- Cell Survival and Cell Death at the Intersection of Autophagy and Apoptosis: Implications for Current and Future Cancer Therapeutics.ACS pharmacology & translational science · 2021Review
- TCP1 increases drug resistance in acute myeloid leukemia by suppressing autophagy via activating AKT/mTOR signaling.Cell death & disease · 2021Article
- WX20120108, a novel IAP antagonist, induces tumor cell autophagy via activating ROS-FOXO pathway.Acta pharmacologica Sinica · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
GDC-0152 is a new type of chemical compound which can downregulate inhibitor of apoptosis protein. We previously reported that GDC-0152 induced apoptosis in HL-60 cells in a caspase-dependent manner. In this study, we have focused on GDC-0152-induced autophagy and the relationship between apoptosis and autophagy. We found that GDC-0152 can evoke autophagy flux as confirmed by the upregulation of LC3 and downregulation of p62. The conversion of LC3I to LC3II verified the existence of autophagy flux further. GDC-0152 induced autophagy through downregulating B cell lymphoma 2 and Bcl-2-interacting myosin-like coiled-coil protein, and upregulating WD-repeat domain phosphoinositide-interacting protein 1. Pretreating HL-60 cells with autophagy inhibitor Bafolimycin A1 reduced GDC-0152-induced apoptosis. However, pretreatment with caspase inhibitor Z-VAD-FMK had no effect on autophagy. Reactive oxygen species were released in GDC-0152-treated HL-60 cells but did not take part in the regulation of autophagy and apoptosis. In conclusion, our findings suggest that GDC-0152-induced autophagy can trigger apoptosis in HL-60 cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.