ArticleAutophagy2015
RIPK1 regulates survival of human melanoma cells upon endoplasmic reticulum stress through autophagy.
Article in Autophagy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 83 citations in OpenAlex.
- Endoplasmic reticulum stress in disease pathogenesis: its implications for therapy.Signal transduction and targeted therapy · 2026Review
- Targeting RIPK1 to modulate cell death and tumour microenvironment in cancer therapy.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- Inhibition of anti-apoptotic Bcl-2 family members promotes synergistic cell death with ER stress inducers by disrupting autophagy in glioblastoma.Cell death discovery · 2025Article
- The role of non-coding RNAs in the regulation of cell death pathways in melanoma.Discover oncology · 2025Review
- The prognostic and neuroendocrine implications of SLC25A29-mediated biomass signature in prostate cancer.GeroScience · 2025Article
- Review
- Specific signaling pathways mediated programmed cell death in tumor microenvironment and target therapies.Discover oncology · 2025Review
- Identification of MAPK12 as a Prognostic Biomarker for Esophageal Carcinoma Using Bioinformatics and Machine Learning.BioMed research international · 2025Article
- Proteome-wide Mendelian randomization and functional studies uncover therapeutic targets for polycystic ovarian syndrome.American journal of human genetics · 2024Article
- Tumorous IRE1α facilitates CD8Cell communication and signaling : CCS · 2024Article
- Electromagnetic Field Stimulation Therapy for Alzheimer's Disease.Neurology (Chicago, Ill.) · 2024Article
- RIPK1 is aberrantly expressed in multiple B-cell cancers and implicated in the underlying pathogenesis.Discover oncology · 2023Article
- SIRT7 orchestrates melanoma progression by simultaneously promoting cell survival and immune evasion via UPR activation.Signal transduction and targeted therapy · 2023Article
- TNFSF10, an autophagy related gene, was a prognostic and immune infiltration marker in skin cutaneous melanoma.Journal of Cancer · 2023Article
- Pan-cancer analysis supports MAPK12 as a potential prognostic and immunotherapeutic target in multiple tumor types, including in THCA.Oncology letters · 2022Article
- Article
- p38MAPK guards the integrity of endosomal compartments through regulating necrotic death.Scientific reports · 2022Article
- Multidimensional insights into the repeated electromagnetic field stimulation and biosystems interaction in aging and age-related diseases.Journal of biomedical science · 2022Review
- MLKL deficiency in BrafCell death & disease · 2022Article
- IKKβ Alleviates Neuron Injury in Alzheimer's Disease via Regulating Autophagy and RIPK1-Mediated Necroptosis.Molecular neurobiology · 2022Article
Corrections and comments
- Erratum issuedCorrigendum.2020
- Erratum issuedCorrection.2022
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although RIPK1 (receptor [TNFRSF]-interacting protein kinase 1) is emerging as a critical determinant of cell fate in response to cellular stress resulting from activation of death receptors and DNA damage, its potential role in cell response to endoplasmic reticulum (ER) stress remains undefined. Here we report that RIPK1 functions as an important prosurvival mechanism in melanoma cells undergoing pharmacological ER stress induced by tunicamycin (TM) or thapsigargin (TG) through activation of autophagy. While treatment with TM or TG upregulated RIPK1 and triggered autophagy in melanoma cells, knockdown of RIPK1 inhibited autophagy and rendered the cells sensitive to killing by TM or TG, recapitulating the effect of inhibition of autophagy. Consistently, overexpression of RIPK1 enhanced induction of autophagy and conferred resistance of melanoma cells to TM- or TG-induced cell death. Activation of MAPK8/JNK1 or MAPK9/JNK2, which phosphorylated BCL2L11/BIM leading to its dissociation from BECN1/Beclin 1, was involved in TM- or TG-induced, RIPK1-mediated activation of autophagy; whereas, activation of the transcription factor HSF1 (heat shock factor protein 1) downstream of the ERN1/IRE1-XBP1 axis of the unfolded protein response was responsible for the increase in RIPK1 in melanoma cells undergoing pharmacological ER stress. Collectively, these results identify upregulation of RIPK1 as an important resistance mechanism of melanoma cells to TM- or TG-induced ER stress by protecting against cell death through activation of autophagy, and suggest that targeting the autophagy-activating mechanism of RIPK1 may be a useful strategy to enhance sensitivity of melanoma cells to therapeutic agents that induce ER stress.
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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.