ArticleOncogene2022
Nuclear translocation of Gasdermin D sensitizes colorectal cancer to chemotherapy in a pyroptosis-independent manner.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Gasdermin-Mediated Pyroptosis: Novel Strategies Against Colorectal Cancer.Cancer science · 2026Review
- Theme and variations: activation and regulation of gasdermin-mediated inflammation.Biochemical Society transactions · 2026Review
- GSDME acts as an epigenetic modifier to promote melanoma development via centriole biogenesis regulator PLK4.Cell death and differentiation · 2026Article
- Pyroptosis as a double-edged sword in colorectal cancer: Molecular mechanisms and therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2026Review
- Proinflammatory GSDMD activation in live macrophages and DLBCL cells marks cognate interactions and better prognosis.Blood advances · 2026Article
- Nuclear gasdermin E drives endothelin-1-induced metastatic progression independently of the pyroptosis.Cell death & disease · 2026Article
- Gasdermins: multifunctional effectors of membrane permeabilization across cellular compartments.The FEBS journal · 2025Review
- Anticancer Effects ofIranian journal of public health · 2025Article
- The TET3 inflammasome senses unique long HSV-1 proteins for virus particle budding from the nucleus.Cellular & molecular immunology · 2024Article
- Gasdermin D promotes development of intestinal tumors through regulating IL-1β release and gut microbiota composition.Cell communication and signaling : CCS · 2024Article
- Research progress on the effect of pyroptosis on the occurrence, development, invasion and metastasis of colorectal cancer.World journal of gastrointestinal oncology · 2024Review
- The gasdermin family: emerging therapeutic targets in diseases.Signal transduction and targeted therapy · 2024Review
- Gasdermin E promotes translocation of p65 and c-jun into nucleus in keratinocytes for progression of psoriatic skin inflammation.Cell death & disease · 2024Article
- Musashi-2 potentiates colorectal cancer immune infiltration by regulating the post-translational modifications of HMGB1 to promote DCs maturation and migration.Cell communication and signaling : CCS · 2024Article
- EGFR-Activated JAK2/STAT3 Pathway Confers Neuroprotection in Spinal Cord Ischemia-Reperfusion Injury: Evidence from High-Throughput Sequencing and Experimental Models.Molecular neurobiology · 2024Article
- The role of pyroptosis and gasdermin family in tumor progression and immune microenvironment.Experimental hematology & oncology · 2023Review
- Musashi-2 Deficiency Triggers Colorectal Cancer Ferroptosis by Downregulating the MAPK Signaling Cascade to Inhibit HSPB1 Phosphorylation.Biological procedures online · 2023Article
- Gasdermins gone wild: new roles for GSDMs in regulating cellular homeostasis.Trends in cell biology · 2023Review
- Gasdermins assemble; recent developments in bacteriology and pharmacology.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gasdermin D (GSDMD) has recently been identified as a cytoplasmic effector protein that plays a central role in pyroptosis of immune cells. However, GSDMD is a universally expressed protein, and its function beyond pyroptosis, especially in cancer cells, has not been well characterized. Here, we report that predominant localization of GSDMD in the nucleoplasm in vivo indicates favorable clinical outcomes in colorectal cancer, while a lack of nuclear localization of GSDMD is associated with poor outcomes. Nuclear GSDMD, rather than cytoplasmic GSDMD, inhibits cell growth and promotes apoptosis in colorectal cancer. Hypoxia in the tumor microenvironment accounts for mild or moderate nuclear translocation of GSDMD in vivo. Under the stimulation of chemotherapy drugs, nuclear GSDMD promotes apoptosis via regulation of its subcellular distribution rather than pyroptosis-related cleavage. After nuclear translocation, GSDMD interacts with PARP-1 to dramatically inhibit its DNA damage repair-related function by functioning like the PARP inhibitor olaparib, thus forming a "hypoxia/chemotherapy-GSDMD nuclear translocation-PARP-1 blockade-DNA damage and apoptosis" axis. This study redefines the pyroptosis-independent function of GSDMD and suggests that the subcellular localization of GSDMD may serve as a molecular indicator of clinical outcomes and a promising therapeutic target in colorectal cancer.
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