ArticleEuropean journal of histochemistry : EJH2021
Overexpression of <em>MYBL2</em> predicts poor prognosis and promotes oncogenesis in endometrial carcinoma.
Article in European journal of histochemistry : EJH, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- FBXW7 Inhibited M2 Macrophage Polarization in Endometrial Cancer by Reducing CCL2 Secretion Through Ubiquitination of MYBL2 Subtitle: The Role of FBXW7 on M2 Macrophage Polarization in EC.Biochemical genetics · 2026Article
- MYBL2 is a Novel Independent Prognostic Biomarker and Correlated with TMB in pancreatic cancer.Journal of Cancer · 2024Article
- Clinical analysis of molecular typing of 146 cases of endometrial carcinoma.Frontiers in oncology · 2024Article
- [High expression of MYBL2 promotes progression and predicts a poor survival outcome of prostate cancer].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Latest developments in the pathobiology of Ewing sarcoma.Journal of bone oncology · 2022Review
- Comprehensive Analysis of the Expression and Prognosis for the DREAM Complex in Human Cancers.Frontiers in genetics · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometrial cancer (EC) is the most common gynecologic malignancy and still remains clinically challenging. We aimed to explore the potential biomarkers of EC and provide a theoretical basis for early screening and targeted therapy. The available transcriptome data from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were analyzed to identify differentially expressed genes. Immunohistochemistry was performed to detect gene expression. We analyzed the associations of MYBL2 with clinicopathological features and survival time and the biological effect of MYBL2 on the proliferation of EC cells. The effect of MYBL2 silencing on the transcriptome of EC cell model was analyzed by RNA-Seq. MYBL2 was significantly upregulated with obvious copy number alteration (CNA) in EC. Copy number amplification significantly increased MYBL2 mRNA expression, which led to a poor prognosis and severe pathological types of EC. Additionally, MYBL2 silencing significantly inhibited proliferation and induced apoptosis and G1-phase cell cycle arrest in EC cell lines. Our results indicate that MYBL2 is closely related to the cell cycle and apoptosis pathways in EC. The findings in this study provide evidence that MYBL2 can serve as a new candidate prognostic marker and a target for future therapeutic intervention in EC.
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