ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Icaritin activates JNK-dependent mPTP necrosis pathway in colorectal cancer cells.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 66 citations in OpenAlex.
- The potential of mitochondrial permeability transition-driven necrosis-related genes in prognostic evaluation of colorectal cancer patients.Frontiers in oncology · 2026Article
- A Novel MPT-Driven Necrosis-Related lncRNA Signature for Prognostic Prediction in Hepatocellular Carcinoma: Validation Using Organoids.Cancer medicine · 2026Article
- Cyclophilin D suppresses colorectal cancer progression through the activation of an autophagy-mediated apoptotic pathway.Scientific reports · 2025Article
- Development of a Mitochondrial Permeability Transition-Driven Necrosis-Related Prognostic Signature in Cervical Cancer: Integrating Bulk Transcriptomic and Single-Cell Data.Cancer medicine · 2025Article
- Icaritin Represses Autophagy to Promote Colorectal Cancer Cell Apoptosis and Sensitized Low-Temperature Photothermal Therapy via Targeting HSP90-TXNDC9 Interactions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Hyaluronic Acid-Functionalized Bismuth Vanadate/Molybdenum Disulfide Nanoheterojunctions Achieve Efficient Phototherapy of Hypoxic Tumor.Biomaterials research · 2025Article
- Targeting POLRMT by IMT1 inhibits colorectal cancer cell growth.Cell death & disease · 2024Article
- Icariin improves oxidative stress injury during ischemic stroke via inhibiting mPTP opening.Molecular medicine (Cambridge, Mass.) · 2024Article
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- Regulated cell death in glioma: promising targets for natural small-molecule compounds.Frontiers in oncology · 2024Review
- Targeting SphK1/2 by SKI-178 inhibits prostate cancer cell growth.Cell death & disease · 2023Article
- Multidisciplinary strategies to enhance therapeutic effects of flavonoids from Epimedii Folium: Integration of herbal medicine, enzyme engineering, and nanotechnology.Journal of pharmaceutical analysis · 2023Review
- Icaritin inhibits PLK1 to activate DNA damage response in NK/T cell lymphoma and increases sensitivity to GELOX regime.Molecular therapy oncolytics · 2022Article
- The sphingosine kinase inhibitor SKI-V suppresses cervical cancer cell growth.International journal of biological sciences · 2022Article
- Cyclophilin D: Guardian or Executioner for Tumor Cells?Frontiers in oncology · 2022Review
- Profiling the chemical nature of anti-oxytotic/ferroptotic compounds with phenotypic screening.Free radical biology & medicine · 2021Article
- AMPK activation by ASP4132 inhibits non-small cell lung cancer cell growth.Cell death & disease · 2021Article
- The Role of Cyclophilins in Inflammatory Bowel Disease and Colorectal Cancer.International journal of biological sciences · 2021Review
- A comparative study on theDrug delivery · 2020Article
- The interaction mechanism between autophagy and apoptosis in colon cancer.Translational oncology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The colorectal cancer (CRC) is one leading contributor of cancer-related mortality worldwide. The search for effective anti-CRC agents is valuable. In the current study, we showed that icaritin (ICT), an active natural ingredient from the Chinese plant Epimedium, potently inhibited proliferation and survival of established (HT-29, HCT-116, DLD-1, and SW-620) and primary (patient-derived) CRC cells. Significantly, ICT mainly induced necrosis, but not apoptosis, in CRC cells. The necrosis inhibitor necrostatin-1 attenuated ICT-mediated cytotoxicity in CRC cells. We showed that ICT treatment in CRC cells induced mitochondrial permeability transition pore (mPTP) opening, which was evidenced by mitochondrial membrane potential (MMP) decrease and mitochondrial adenine nucleotide translocator-1 (ANT-1)-cyclophilin-D (CyPD) association. On the other hand, mPTP blockers, including sanglifehrin A, cyclosporin A, and bongkrekic acid, as well as siRNA-mediated knockdown of mPTP component (CyPD or ANT-1), significantly alleviated ICT-mediated cytotoxicity against CRC cells. We suggested that Jun-N-terminal kinase (JNK) activation by ICT mediated mPTP opening and subsequent CRC cell necrosis. JNK pharmacological inhibition, dominant negative mutation, or shRNA downregulation suppressed ICT-induced MMP reduction and subsequent HT-29 cell necrosis. In vivo, oral gavage of ICT dramatically inhibited HT-29 xenograft growth in nude mice. The in vivo activity by ICT was largely attenuated by co-administration with the mPTP blocker CsA. Collectively, our results showed that ICT exerts potent inhibitory effect against CRC cells in vitro and in vivo. JNK-dependent mPTP necrosis pathway could be key mechanism responsible for ICT's actions.
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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.