ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2014
Triptolide activates unfolded protein response leading to chronic ER stress in pancreatic cancer cells.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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Who cites it
34 citing papers in PubMed, 47 citations in OpenAlex.
- GRP78 dysregulation: A proposed molecular mechanism linking the tumor microenvironment to sepsis susceptibility in patients with cancer (Review).International journal of molecular medicine · 2026Review
- Natural Products in Cancer Research: Mechanistic Advances, Translational Challenges, and the Emerging Role of Chilean Biodiversity.Molecules (Basel, Switzerland) · 2026Review
- Pharmacological activation of SERCA2 reverses ER calcium dysregulation and depression-like behaviors in hyperglycemic mice.Scientific reports · 2025Article
- Modulation of endoplasmic reticulum stress-induced insulin resistance by the low-carbohydrate high-fat ketogenic diet.Frontiers in nutrition · 2025Review
- Review
- Article
- Insights from the molecular docking analysis of GRP78 with natural compound inhibitors in the management of cancers.Bioinformation · 2023Article
- Increasing Stress to Induce Apoptosis in Pancreatic Cancer via the Unfolded Protein Response (UPR).International journal of molecular sciences · 2022Review
- Protective Effect of XinJiaCongRongTuSiZiWan on the Reproductive Toxicity of Female Rats Induced by Triptolide.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Novel compound C150 inhibits pancreatic cancer through induction of ER stress and proteosome assembly.Frontiers in oncology · 2022Article
- Natural Products Targeting ER Stress, and the Functional Link to Mitochondria.International journal of molecular sciences · 2020Review
- Targeting the GRP78 Pathway for Cancer Therapy.Frontiers in medicine · 2020Review
- 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
- Induction of endoplasmic reticulum stress by aminosteroid derivative RM-581 leads to tumor regression in PANC-1 xenograft model.Investigational new drugs · 2019Article
- Triptolide, A Potential Autophagy Modulator.Chinese journal of integrative medicine · 2019Review
- ER stress sensor, glucose regulatory protein 78 (GRP78) regulates redox status in pancreatic cancer thereby maintaining "stemness".Cell death & disease · 2019Article
- GRP78-mediated antioxidant response and ABC transporter activity confers chemoresistance to pancreatic cancer cells.Molecular oncology · 2018Article
- Inhibition of endoplasmic-reticulum-stress-mediated autophagy enhances the effectiveness of chemotherapeutics on pancreatic cancer.Journal of translational medicine · 2018Article
- SERP1 is a novel marker of poor prognosis in pancreatic ductal adenocarcinoma patients via anti-apoptosis and regulating SRPRB/NF-κB axis.International journal of oncology · 2017Article
- "Heat shock protein 70 in pancreatic diseases: Friend or foe".Journal of surgical oncology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Pancreatic cancer is a devastating disease with a survival rate of <5%. Moreover, pancreatic cancer aggressiveness is closely related to high levels of prosurvival mediators, which can ultimately lead to rapid disease progression. One of the mechanisms that enables tumor cells to evade cellular stress and promote unhindered proliferation is the endoplasmic reticulum (ER) stress response. Disturbances in the normal functions of the ER lead to an evolutionarily conserved cell stress response, the unfolded protein response (UPR). The UPR initially compensates for damage, but it eventually triggers cell death if ER dysfunction is severe or prolonged. Triptolide, a diterpene triepoxide, has been shown to be an effective compound against pancreatic cancer. Our results show that triptolide induces the UPR by activating the PKR-like ER kinase-eukaryotic initiation factor 2α axis and the inositol-requiring enzyme 1α-X-box-binding protein 1 axis of the UPR and leads to chronic ER stress in pancreatic cancer. Our results further show that glucose-regulated protein 78 (GRP78), one of the major regulators of ER stress, is downregulated by triptolide, leading to cell death by apoptosis in MIA PaCa-2 cells and autophagy in S2-VP10 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.