ArticleOncotarget2015
JNK suppression of chemotherapeutic agents-induced ROS confers chemoresistance on pancreatic cancer stem cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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.
The trial behind it
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Who cites it
51 citing papers in PubMed, 94 citations in OpenAlex.
- The role of NLRP3 inflammasome in 5-fluorouracil resistance of oral squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2017Trial
- Musashi-1 Drives Radioresistance and Stemness in Head and Neck Squamous Cell Carcinoma via a Radioresistant FaDu Model.Cancer science · 2026Article
- Pharmacological Inhibition of JNK Signalling Exerts Anti-Neoplastic Effects on SH-SY5Y Human Neuroblastoma Cells.International journal of molecular sciences · 2025Article
- Beyond endocrine resistance: estrogen receptor (ESR1) activating mutations mediate chemotherapy resistance through the JNK/c-Jun MDR1 pathway in breast cancer.Breast cancer research and treatment · 2025Article
- Combining gemcitabine and MSC delivering soluble TRAIL to target pancreatic adenocarcinoma and its stroma.Cell reports. Medicine · 2024Article
- Deciphering cellular plasticity in pancreatic cancer for effective treatments.Cancer metastasis reviews · 2024Review
- Auraptene-induced cytotoxic effects in acute myeloid leukemia cell lines.Medical oncology (Northwood, London, England) · 2023Article
- Reshaping the Pancreatic Cancer Microenvironment at Different Stages with Chemotherapy.Cancers · 2023Review
- Target c-Myc to treat pancreatic cancer.Cancer biology & therapy · 2022Article
- Modulation of Reactive Oxygen Species to Overcome 5-Fluorouracil Resistance.Biomolecules & therapeutics · 2022Review
- Construction of immune-related lncRNA signature to predict aggressiveness, immune landscape, and drug resistance of colon cancer.BMC gastroenterology · 2022Article
- HNMT Upregulation Induces Cancer Stem Cell Formation and Confers Protection against Oxidative Stress through Interaction with HER2 in Non-Small-Cell Lung Cancer.International journal of molecular sciences · 2022Article
- Role of the JNK Pathway in Bladder Cancer.OncoTargets and therapy · 2022Review
- The MK2/Hsp27 axis is a major survival mechanism for pancreatic ductal adenocarcinoma under genotoxic stress.Science translational medicine · 2021Article
- Dexamethasone Sensitizes Cancer Stem Cells to Gemcitabine and 5-Fluorouracil by Increasing Reactive Oxygen Species Production through NRF2 Reduction.Life (Basel, Switzerland) · 2021Article
- Stress-activated kinases as therapeutic targets in pancreatic cancer.World journal of gastroenterology · 2021Review
- ROS and TGFβ: from pancreatic tumour growth to metastasis.Journal of experimental & clinical cancer research : CR · 2021Review
- JNK signaling as a target for anticancer therapy.Pharmacological reports : PR · 2021Review
- Therapeutic targeting of pancreatic cancer stem cells by dexamethasone modulation of the MKP-1-JNK axis.The Journal of biological chemistry · 2020Article
- Anti-Proliferative Effect ofMolecules (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemoresistance associated with cancer stem cells (CSCs), which is now being held responsible for the pervasive therapy resistance of pancreatic cancer, poses a major challenge to the successful management of this devastating malignancy. However, the molecular mechanism underlying the marked chemoresistance of pancreatic CSCs remains largely unknown. Here we show that JNK, which is upregulated in pancreatic CSCs and contributes to their maintenance, is critically involved in the resistance of pancreatic CSCs to 5-fluorouracil (5-FU) and gemcitabine (GEM). We found that JNK inhibition effectively sensitizes otherwise chemoresistant pancreatic CSCs to 5-FU and GEM. Significantly, JNK inhibition promoted 5-FU- and GEM-induced increase in intracellular reactive oxygen species (ROS), and scavenging intracellular ROS by use of N-acetylcysteine impaired JNK inhibition-mediated promotion of the cytotoxicity of 5-FU and GEM. Our findings thus suggest that JNK may contribute to the chemoresistance of pancreatic CSCs through prevention of chemotherapeutic agents-induced increase in intracellular ROS. Our findings also suggest that JNK inhibition combined with 5-FU- and/or GEM-based regimens may be a rational therapeutic approach to effectively eliminate pancreatic CSCs.
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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.