ArticleCell death discovery2017
Matrine induces RIP3-dependent necroptosis in cholangiocarcinoma cells.
Article in Cell death discovery, 2017. 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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The trial behind it
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Who cites it
33 citing papers in PubMed, 56 citations in OpenAlex.
- Programmed cell death in cancer: targeting necroptosis to kill tumor cell.Cell death discovery · 2026Review
- The necroptosis-related lncRNA ENSG00000253385.1 promotes the progression of esophageal squamous cell carcinoma by targeting the miR-16-2-3p/VDAC1 axis.Scientific reports · 2025Article
- Novel isobavachalcone derivatives induce apoptosis and necroptosis in human non-small cell lung cancer H1975 cells.Journal of enzyme inhibition and medicinal chemistry · 2024Article
- Traditional Chinese medicine for the treatment of cancers of hepatobiliary system: from clinical evidence to drug discovery.Molecular cancer · 2024Review
- Efficacy and Safety of Asparagusic Acid againstTropical medicine and infectious disease · 2024Article
- Current evidence and therapeutic implication of PANoptosis in cancer.Theranostics · 2024Review
- Targeting programmed cell death via active ingredients from natural plants: a promising approach to cancer therapy.Frontiers in pharmacology · 2024Review
- A pilot in vivo study: potential ovarian cancer therapeutic by placental extracellular vesicles.Bioscience reports · 2023Article
- Identification of a necroptosis-related gene signature as a novel prognostic biomarker of cholangiocarcinoma.Frontiers in immunology · 2023Article
- Necroptosis: A Pathogenic Negotiator in Human Diseases.International journal of molecular sciences · 2022Review
- Non-apoptotic cell death-based cancer therapy: Molecular mechanism, pharmacological modulators, and nanomedicine.Acta pharmaceutica Sinica. B · 2022Review
- Identification and validation of necroptosis-related prognostic gene signature and tumor immune microenvironment infiltration characterization in esophageal carcinoma.BMC gastroenterology · 2022Article
- Targeting Drug Chemo-Resistance in Cancer Using Natural Products.Biomedicines · 2021Review
- MiRNA-124 regulates the sensitivity of renal cancer cells to cisplatin-induced necroptosis by targeting the CAPN4-CNOT3 axis.Translational andrology and urology · 2021Article
- Review
- Receptor-interacting protein in malignant digestive neoplasms.Journal of Cancer · 2021Review
- RIP3 mediates TCN-induced necroptosis through activating mitochondrial metabolism and ROS production in chemotherapy-resistant cancers.American journal of cancer research · 2021Article
- Review
- Targeting necroptosis in anticancer therapy: mechanisms and modulators.Acta pharmaceutica Sinica. B · 2020Review
- Necroptosis in Cholangiocarcinoma.Cells · 2020Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of acquired resistance to pro-apoptotic antitumor agents is a major impediment to the cure of cholangiocarcinoma (CCA). Antitumor drugs inducing non-apoptotic cell death are considered as a new approach to overcome such drug resistance. Here, we reported for the first time that matrine-induced necroptosis in CCA cell lines, differing from its classical role to induce apoptosis in many other kinds of cancer cells. CCA cells under matrine treatment exhibited typical necrosis-like but not apoptotic morphologic change. These matrine-induced morphologic change and cell death in CCA cells were greatly attenuated by necroptosis inhibitor necrostatin-1, but not apoptosis inhibitor z-VAD-fmk. Unlike many cancer cells with negative receptor-interacting protein 3 (RIP3) expression, moderate expression of RIP3 in CCA cells was observed and was required for matrine to induce necroptosis, which was switched to apoptosis after knocking down endogenous RIP3. Moreover, matrine could increase RIP3 expression level, which may facilitate the necroptosis process. Translocation of mixed lineage kinase-domain like (MLKL) from cytoplasm to plasma membrane as a downstream event of RIP3, as well as the increased production of reactive oxygen species (ROS) by RIP3/MLKL, was critical for matrine to induce necroptosis. In clinical study, we found RIP3 was lower but still moderately expressed in most CCA tissue samples compared with adjacent normal tissues. Taken together, we identified matrine as a necroptosis inducer in CCA by enhancing RIP3 expression and the following RIP3/MLKL/ROS signaling pathway, which provided new individualized strategies based on RIP3 expression to overcome chemoresistance in CCA therapy.
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What OpenQuestion holds
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.