ArticleCell death & disease2021
The MYEOV-MYC association promotes oncogenic miR-17/93-5p expression in pancreatic ductal adenocarcinoma.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- MYC in Oncogenesis and Therapeutic Implications.MedComm · 2026Review
- A TRPM4-associated necrotic cell death signature for prognostic stratification in pancreatic cancer.Journal of gastrointestinal oncology · 2026Article
- MYEOV Is a Novel Marker of Differentiated Corneal Epithelium.Investigative ophthalmology & visual science · 2025Article
- The role of MYEOV gene: a review and future directions.Frontiers in oncology · 2025Review
- Repression of YEATS2 induces cellular senescence in hepatocellular carcinoma and inhibits tumor growth.Cell cycle (Georgetown, Tex.) · 2024Article
- Evolutionarily conserved enhancer-associated features within theFrontiers in cell and developmental biology · 2024Article
- Exosomal miRNA Biomarker Panel for Pancreatic Ductal Adenocarcinoma Detection in Patient Plasma: A Pilot Study.International journal of molecular sciences · 2023Article
- Article
- mCells · 2022Article
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
Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy worldwide. As metastasis and malignant progression are primarily responsible for the poor clinical outcomes of PDAC, identifying key genes involved in these processes and the underlying molecular mechanisms of PDAC is vital. In this study, by analyzing TCGA PDAC data and matched GTEx data, we found that MYEOV expression is associated with poor survival in PDAC patients and higher in carcinoma tissues than in healthy tissues. Elevated levels of MYEOV led to enhanced cell proliferation, invasion and migration in vitro and in vivo. Transcriptome analysis results revealed that MYEOV mediates global alterations in gene expression profiles in PDAC cells. MiRNA-seq analysis showed that MYEOV regulates the expression levels of miR-17-5p and miR-93-5p, and its depletion resulted in reduced cell proliferation, invasion and migration, as observed in MYEOV-knockdown PDAC cells. These effects are likely due to the ability of MYEOV to regulate enrichment of the transcription factor MYC at the gene promoter regions of the two miRNAs. Furthermore, we identified a complex containing MYEOV and MYC in the nucleus, providing additional evidence for the association of MYEOV with MYC. Taken together, our results suggest that MYEOV promotes oncogenic miR-17/93-5p expression by associating with MYC, contributing to PDAC progression.
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