ArticleOncotarget2015
YM155, a survivin suppressant, triggers PARP-dependent cell death (parthanatos) and inhibits esophageal squamous-cell carcinoma xenografts in mice.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The trial behind it
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- Striking at Survivin: YM-155 Inhibits High-Risk Neuroblastoma Growth and Enhances Chemosensitivity.Cancers · 2025Article
- Apoptosis-inducing factor (AIF) at the crossroad of cell survival and cell death: implications for cancer and mitochondrial diseases.Cell communication and signaling : CCS · 2025Review
- Specific signaling pathways mediated programmed cell death in tumor microenvironment and target therapies.Discover oncology · 2025Review
- Parthanatos and apoptosis: unraveling their roles in cancer cell death and therapy resistance.EXCLI journal · 2025Review
- CHD1L Regulates Cell Survival in Breast Cancer and Its Inhibition by OTI-611 Impedes the DNA Damage Response and Induces PARthanatos.International journal of molecular sciences · 2024Article
- Emerging role of immunogenic cell death in cancer immunotherapy.Frontiers in immunology · 2024Review
- The cardiac glycoside ZINC253504760 induces parthanatos-type cell death and G2/M arrest via downregulation of MEK1/2 phosphorylation in leukemia cells.Cell biology and toxicology · 2023Article
- Molecular Mechanisms of Parthanatos and Its Role in Diverse Diseases.International journal of molecular sciences · 2022Review
- Inhibition of AKT induces p53/SIRT6/PARP1-dependent parthanatos to suppress tumor growth.Cell communication and signaling : CCS · 2022Article
- Generation of reactive oxygen species is the primary mode of action and cause of survivin suppression by sepantronium bromide (YM155).RSC medicinal chemistry · 2021Article
- YM155 sensitizes HeLa cells to TRAIL-mediated apoptosis via cFLIP and survivin downregulation.Oncology letters · 2020Article
- Sevoflurane Exposure Induces Neuronal Cell Parthanatos Initiated by DNA Damage in the Developing Brain via an Increase of Intracellular Reactive Oxygen Species.Frontiers in cellular neuroscience · 2020Article
- Caspase-Independent Regulated Necrosis Pathways as Potential Targets in Cancer Management.Frontiers in oncology · 2020Review
- YM155 enhances the cytotoxic activity of etoposide against canine osteosarcoma cells.The Journal of veterinary medical science · 2019Article
- Mutant p53 increases exosome-mediated transfer of miR-21-3p and miR-769-3p to promote pulmonary metastasis.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2019Article
- The dual role of poly(ADP-ribose) polymerase-1 in modulating parthanatos and autophagy under oxidative stress in rat cochlear marginal cells of the stria vascularis.Redox biology · 2018Article
- Clinicopathological and functional implications of the inhibitor of apoptosis proteins survivin and XIAP in esophageal cancer.Oncology letters · 2018Article
- Overexpression of stathmin plays a pivotal role in the metastasis of esophageal squamous cell carcinoma.Oncotarget · 2017Article
- JNK Activation Contributes to Oxidative Stress-Induced Parthanatos in Glioma Cells via Increase of Intracellular ROS Production.Molecular neurobiology · 2017Article
- YM155 enhances ABT-737-mediated apoptosis through Mcl-1 downregulation in Mcl-1-overexpressed cancer cells.Molecular and cellular biochemistry · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here we demonstrated that sepantronium bromide (YM155), a survivin suppressant, inhibited esophageal squamous-cell carcinoma (ESCC) growth in mice bearing human ESCC xenografts without affecting body weight. In cell culture, YM155 decreased survivin levels and caused PARP-1 activation, poly-ADP polymer formation, and AIF translocation from the cytosol to the nucleus. Genetic knockdown of PARP-1 or AIF abrogated YM155-induced parthanatos cell death. Furthermore, FOS, JUN and c-MYC gene transcription, which is stimulated by activated PARP-1, was increased following YM155 treatment. Our data demonstrate that YM155 did not trigger apoptosis, but induced parthanatos, a cell death dependent on PARP-1 hyper-activation, and support clinical development of YM155 in ESCC.
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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.