Open AccessOverexpression of <em>MYBL2</em> predicts poor prognosis and promotes oncogenesis in endometrial carcinoma
Author(s) -
Lulu Le,
Ji Luo,
Huimeng Wu,
Ling Chen,
Xiaoli Tang,
Fang Fu
Publication year - 2021
Publication title -
european journal of histochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.754
H-Index - 42
eISSN - 2038-8306
pISSN - 1121-760X
DOI - 10.4081/ejh.2021.3226
Subject(s) - carcinogenesis , gene silencing , transcriptome , cell cycle , cancer research , biology , downregulation and upregulation , medicine , endometrial cancer , bioinformatics , oncology , cancer , gene expression , gene , genetics
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.