ArticleInternational journal of molecular medicine2018
DPY30 is required for the enhanced proliferation, motility and epithelial-mesenchymal transition of epithelial ovarian cancer cells.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 20 citations in OpenAlex.
- The Bidirectional Role of Cellular Senescence in the Treatment of Ovarian Cancer.Biomedicines · 2026Review
- Set1 promotes Notch-induced transcriptional activation.Cellular and molecular life sciences : CMLS · 2026Article
- Epigenetics in Ovarian Cancer: A Review of Current Knowledge and Future Perspectives.Biomedicines · 2025Review
- The role of chromatin modulator DPY30 in glucose metabolism of colorectal cancer cells.Translational cancer research · 2024Article
- DPY30 knockdown suppresses colorectal carcinoma progression via inducing Raf1/MST2-mediated apoptosis.Heliyon · 2024Article
- DPY30 promotes colorectal carcinoma metastasis by upregulating ZEB1 transcriptional expression.Cancer cell international · 2023Article
- Identification and validation of DPY30 as a prognostic biomarker and tumor immune microenvironment infiltration characterization in esophageal cancer.Oncology letters · 2023Article
- DPY30 promotes the growth and survival of osteosarcoma cell by regulating the PI3K/AKT signal pathway.European journal of histochemistry : EJH · 2023Article
- DPY30 Promotes Proliferation and Cell Cycle Progression of Colorectal Cancer Cells via Mediating H3K4 Trimethylation.International journal of medical sciences · 2023Article
- Mass spectroscopy-based proteomics and metabolomics analysis of triple-positive breast cancer cells treated with tamoxifen and/or trastuzumab.Cancer chemotherapy and pharmacology · 2022Article
- DPY30 acts as an ASH2L-specific stabilizer to stimulate the enzyme activity of MLL family methyltransferases on different substrates.iScience · 2022Article
- Article
- Next Generation Plasma Proteomics Identifies High-Precision Biomarker Candidates for Ovarian Cancer.Cancers · 2022Article
- The DPY30-H3K4me3 Axis-Mediated PD-L1 Expression in Melanoma.Journal of inflammation research · 2022Article
- ABHD5 inhibits YAP-induced c-Met overexpression and colon cancer cell stemness via suppressing YAP methylation.Nature communications · 2021Article
- The Analysis of Gene Expression Data Incorporating Tumor Purity Information.Frontiers in genetics · 2021Article
- Aberrant Activity of Histone-Lysine N-Methyltransferase 2 (KMT2) Complexes in Oncogenesis.International journal of molecular sciences · 2020Review
- The complex activities of the SET1/MLL complex core subunits in development and disease.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial ovarian cancer (EOC) is one of the most lethal gynecological malignancies and is known to be associated with the accumulation of various genetic and epigenetic alterations. As a member of the human histone‑lysine N‑methyltransferase SETD1A (SET1)/histone‑lysine N‑methyltransferase 2A (MLL) complexes that are required for full SET1/MLL methyltransferase activity, protein dpy‑30 homolog (DPY30) catalyzes histone H3K4 methylation, and its dysfunction has been associated with the occurrence of cancer. Therefore, the present study investigated the role of DPY30 in EOC and the potential association between DPY30 expression and the clinicopathological characteristics of EOC. The expression of DPY30 was examined in EOC tissues and cell lines to identify any correlations between the clinicopathological characteristics of EOC and DPY30 expression, and to determine the effects of DPY30 on EOC cell proliferation, migration and invasion. DPY30 was highly expressed in EOC tissues and cell lines, and high DPY30 expression was significantly associated with notable clinicopathological variables in EOC patients, including International Federation of Gynecology and Obstetrics stage, pathological grade and lymph node metastasis. Functional studies on EOC cell lines demonstrated that DPY30 significantly promoted cell proliferation, migration, and invasion, accelerated cell cycle progression, and promoted epithelial‑mesenchymal transition. Chromatin immunoprecipitation assay results revealed that DPY30 regulates histone H3K4 modification via interaction with the vimentin gene promoter, suggesting that DPY30 promotes the transcription of vimentin. Finally, high expression of DPY30 was significantly associated with reduced survival in patients with EOC. The results indicated that DPY30 may act as an oncogene in EOC and thus represents a potential therapeutic target and prognostic marker in EOC.
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