ArticleCancer biology & therapy2018
Autophagy as a mechanism of Apo2L/TRAIL resistance.
Article in Cancer biology & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- The autophagic protein FYCO1 controls TNFRSF10/TRAIL receptor induced apoptosis and is inactivated by CASP8 (caspase 8).Autophagy · 2023Article
- Mechanism and Role of Endoplasmic Reticulum Stress in Osteosarcoma.Biomolecules · 2022Review
- Review
- Caspase-8 Deficient Osteoblastic Cells Display Alterations in Non-Apoptotic Pathways.Frontiers in cell and developmental biology · 2022Article
- Chemoprotective and chemosensitizing effects of apigenin on cancer therapy.Cancer cell international · 2021Review
- Targeting the ESCRT-III component CHMP2A for noncanonical Caspase-8 activation on autophagosomal membranes.Cell death and differentiation · 2021Article
- TP53INP2 at the crossroad of apoptosis and autophagy in death receptor signaling.Molecular & cellular oncology · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Apo2 ligand (Apo2L)/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is unique to selectively induce apoptosis in tumor cells while sparing normal cells. Thus there is tremendous interest in Apo2L/TRAIL therapy; however, drug resistance is a serious limitation. Autophagy is a cellular housekeeping process that controls protein and organelle turnover, and is almost consistently activated in response to apoptosis-inducing stimuli, including Apo2L/TRAIL. Unlike apoptosis, autophagy leads to cell death or survival depending on the context. Various molecular mechanisms by which autophagy regulates Apo2L/TRAIL-induced apoptosis have been identified. Further, whether autophagy is completed (intact autophagic flux) or not could determine the fate of cancer cells, either cell survival or death. Thus, targeting autophagy is an attractive strategy to overcome Apo2L/TRAIL resistance. We present the current view of how these regulatory mechanisms of this interplay between autophagy and apoptosis may dictate cancer cell response to Apo2L/TRAIL therapy.
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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 Socratic graph.