ArticleExperimental cell research2015
Celastrol induces unfolded protein response-dependent cell death in head and neck cancer.
Article in Experimental cell research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 58 citations in OpenAlex.
- Withaferin A and Celastrol Overwhelm Proteostasis.International journal of molecular sciences · 2023Review
- The synthetic oleanane triterpenoid CDDO-2P-Im binds GRP78/BiP to induce unfolded protein response-mediated apoptosis in myeloma.Molecular oncology · 2023Article
- Induction of the ER stress response in NRVMs is linked to cardiotoxicity caused by celastrol.Acta biochimica et biophysica Sinica · 2022Article
- Histone deacetylase 6 inhibition restores leptin sensitivity and reduces obesity.Nature metabolism · 2022Article
- HTS Identification of Activators and Inhibitors of Endoplasmic Reticulum (ER) Stress and the Unfolded Protein Response (UPR).Methods in molecular biology (Clifton, N.J.) · 2022Article
- The Potential Therapeutic Role of Celastrol in Patients With Heart Failure With Preserved Ejection Fraction.Frontiers in cardiovascular medicine · 2021Review
- Article
- Endoplasmic Reticulum Stress Pathway, the Unfolded Protein Response, Modulates Immune Function in the Tumor Microenvironment to Impact Tumor Progression and Therapeutic Response.International journal of molecular sciences · 2019Review
- Deep insights into the response of human cervical carcinoma cells to a new cyano enone-bearing triterpenoid soloxolone methyl: a transcriptome analysis.Oncotarget · 2019Article
- Targeting the unfolded protein response in head and neck and oral cavity cancers.Experimental cell research · 2019Review
- CaBritish journal of pharmacology · 2019Article
- Impact and Relevance of the Unfolded Protein Response in HNSCC.International journal of molecular sciences · 2019Review
- Identification of Portimine B, a New Cell Permeable Spiroimine That Induces Apoptosis in Oral Squamous Cell Carcinoma.ACS medicinal chemistry letters · 2019Article
- Celastrol inhibits colorectal cancer through TGF-β1/Smad signaling.OncoTargets and therapy · 2019Article
- Interferon γ suppresses dentin sialophosphoprotein in oral squamous cell carcinoma cells resulting in antitumor effects, via modulation of the endoplasmic reticulum response.International journal of oncology · 2018Article
- Anticancer effect of salidroside reduces viability through autophagy/PI3K/Akt and MMP-9 signaling pathways in human bladder cancer cells.Oncology letters · 2018Article
- Novel Low-Toxic Derivative of Celastrol Maintains Protective Effect against Acute Renal Injury.ACS omega · 2018Article
- A Mechanistic Overview of Triptolide and Celastrol, Natural Products fromFrontiers in pharmacology · 2018Review
- Celastrol induces apoptosis in hepatocellular carcinoma cells via targeting ER-stress/UPR.Oncotarget · 2017Article
- Nascent RNA sequencing reveals a dynamic global transcriptional response at genes and enhancers to the natural medicinal compound celastrol.Genome research · 2017Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
The survival rate for patients with oral squamous cell carcinoma (OSCC) has not seen marked improvement in recent decades despite enhanced efforts in prevention and the introduction of novel therapies. We have reported that pharmacological exacerbation of the unfolded protein response (UPR) is an effective approach to killing OSCC cells. The UPR is executed via distinct signaling cascades whereby an initial attempt to restore folding homeostasis in the endoplasmic reticulum during stress is complemented by an apoptotic response if the defect cannot be resolved. To identify novel small molecules able to overwhelm the adaptive capacity of the UPR in OSCC cells, we engineered a complementary cell-based assay to screen a broad spectrum of chemical matter. Stably transfected CHO-K1 cells that individually report (luciferase) on the PERK/eIF2α/ATF4/CHOP (apoptotic) or the IRE1/XBP1 (adaptive) UPR pathways, were engineered [1]. The triterpenoids dihydrocelastrol and celastrol were identified as potent inducers of UPR signaling and cell death in a primary screen and confirmed in a panel of OSCC cells and other cancer cell lines. Biochemical and genetic assays using OSCC cells and modified murine embryonic fibroblasts demonstrated that intact PERK-eIF2-ATF4-CHOP signaling is required for pro-apoptotic UPR and OSCC death following celastrol treatment.
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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.