ArticleCell discovery2023
A RIPK3-independent role of MLKL in suppressing parthanatos promotes immune evasion in hepatocellular carcinoma.
Article in Cell discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 49 citations in OpenAlex.
- Review
- Mechanistic analysis of MLKL-driven cell survival.Cell death discovery · 2026Review
- Regulated cell death programs shaping cancer therapy.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Curcumin induces and enhances the PARP1-mediated parthanatos in diffuse large B cell lymphoma.Oncology letters · 2026Article
- Programmed cell death in lung cancer: mechanisms, immune responses, and therapeutics.Apoptosis : an international journal on programmed cell death · 2026Review
- Regulated necrosis at the crossroads of liver inflammation and cancer development.Nature reviews. Gastroenterology & hepatology · 2026Review
- Cancer neuroscience: signaling pathways and new therapeutic strategies for cancer.Signal transduction and targeted therapy · 2026Review
- MLKL in liver parenchymal cells promotes liver cancer in murine metabolic dysfunction-associated steatotic liver disease.Cell death & disease · 2026Article
- LncRNA OTUD6B-AS1 overexpression induces parthanatos in esophageal adenocarcinoma cells by binding to miR-145-5p and promoting AIF expression.American journal of translational research · 2026Article
- Construction and validation of risk models of prognostic genes associated with parthanatos in papillary thyroid carcinoma based on bioinformatics.Discover oncology · 2025Article
- DCAF13 Regulates Cell Proliferation and Immune Escape of Hepatocellular Carcinoma Through Activating the NF-κB Pathway.Cell biochemistry and biophysics · 2025Article
- Mixed Lineage Kinase Domain-Like Protein (MLKL): From Mechanisms to Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Epigenetic Inactivation of RIPK3-Dependent Necroptosis Augments Cisplatin Chemoresistance in Human Osteosarcoma.International journal of molecular sciences · 2025Article
- Mixed lineage kinase domain-like protein in liver diseases: Cell-type-specific functions and dual roles.World journal of gastroenterology · 2025Article
- Targeting mixed lineage kinase domain-like protein's non-necroptosis role: A new horizon in anti-inflammatory therapy for alcoholic liver disease.World journal of gastroenterology · 2025Article
- Sodium Butyrate Inhibits Necroptosis by Regulating MLKL via E2F1 in Intestinal Epithelial Cells of Liver Cirrhosis.Journal of clinical and translational hepatology · 2025Article
- Prognostic model development using novel genetic signature associated with adenosine metabolism and immune status for patients with hepatocellular carcinoma.Journal of physiology and biochemistry · 2025Article
- MLKL as an emerging machinery for modulating organelle dynamics: regulatory mechanisms, pathophysiological significance, and targeted therapeutics.Frontiers in pharmacology · 2025Review
- Immune checkpoint inhibitors in hepatocellular carcinoma therapy: resistance mechanisms, liver transplantation challenges and management strategies.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Multi-omics analysis of parthanatos related molecular subgroup and prognostic model development in stomach adenocarcinoma.PloS one · 2025Article
Corrections and comments
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Authors and funding
25 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mixed lineage kinase domain-like (MLKL) is widely accepted as an executioner of necroptosis, in which MLKL mediates necroptotic signaling and triggers cell death in a receptor-interacting protein kinase 3 (RIPK3)-dependent manner. Recently, it is increasingly noted that RIPK3 is intrinsically silenced in hepatocytes, raising a question about the role of MLKL in hepatocellular carcinoma (HCC). This study reports a previously unrecognized role of MLKL in regulating parthanatos, a programmed cell death distinct from necroptosis. In HCC cells with intrinsic RIPK3 deficiency, knockout of MLKL impedes the orthotopic tumor growth, activates the anti-tumor immune response and enhances the therapeutic effect of immune checkpoint blockade in syngeneic HCC tumor models. Mechanistically, MLKL is required for maintaining the endoplasmic reticulum (ER)-mitochondrial Mg
Identifiers
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.