ArticleOncogene2025
ZMYND8 promotes the Warburg effect and tumorigenesis through c-Myc activation in pancreatic cancer.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Targeting the Warburg Effect in Anaplastic Thyroid Carcinoma: Metabolic Vulnerabilities and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- The chromatin reader ZMYND8 recruits the NuRD component GATAD2A through its MYND domain to regulate MAPT213 long noncoding RNA transcription.The Journal of biological chemistry · 2026Article
- Single-cell and spatial profiling of peripheral blood and synovium unveils pro-arthritis CNBPJournal of translational medicine · 2026Article
- Lactylation in cancer: mechanistic insights, tumor microenvironment, and therapeutic horizons.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Pancreatic cancer (PC) is a digestive tract tumour with an extremely poor patient prognosis and prominent metabolic abnormalities. However, the molecular mechanisms underlying metabolic reprogramming in the progression of pancreatic cancer remain poorly understood. Here, we employed an epigenetic siRNA library to identify a crucial regulator, ZMYND8, which is involved in glycolysis in PC cells. ZMYND8 was frequently overexpressed in both PC tissues and cell lines, and its elevated expression was significantly correlated with poor overall survival in patients with PC. The high rates of glucose uptake and lactate secretion conferred by ZMYND8 revealed an abnormal activity of aerobic glycolysis in PC cells. Functional studies revealed that ZMYND8 significantly promoted the proliferation, migration and invasion of PC cells. Integrated analyses of CUT&Tag and RNA-seq data revealed that ZMYND8 may activate c-Myc transcriptional activity by modulating downstream epigenetic regulatory pathways. Proteomic profiling and coimmunoprecipitation (Co-IP) assays further demonstrated a direct physical interaction between ZMYND8 and c-Myc. Mechanistic studies revealed that ZMYND8 interacted with and activated c-Myc, thereby promoting the Warburg effect and facilitating PC cell malignancy. Moreover, in vivo studies revealed that overexpression of ZMYND8 resulted in accelerated tumour growth in PC xenografts, which was reversible through the knockdown of c-Myc or treatment with 2-deoxy-D-glucose. Collectively, our data suggest that ZMYND8 functions as a critical metabolic regulator in PC cells by tightly regulating c-Myc activity and may represent a promising novel therapeutic target for advanced pancreatic cancer treatment.
Indexed as
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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.