Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological evidence suggests that elevated androgen levels and genetic variation related to the androgen receptor (AR) increase the risk of endometrial cancer (EC). However, the role of AR in EC is poorly understood. We report that two members of the histone demethylase KDM4 family act as major regulators of AR transcriptional activityin EC. In the MFE-296 cell line, KDM4B and AR upregulate c-myc expression, while in AN3CA cells KDM4A and AR downregulate p27kip1. Additionally, KDM4B expression is positively correlated with AR expression in EC cell lines with high baseline AR expression, while KDM4A and AR expression are positively correlated in low-AR cell lines. In clinical specimens, both KDM4B and KDM4A expression are significantly higher in EC tissues than that in normal endometrium. Finally, patients with alterations in AR, KDM4B, KDM4A, and c-myc have poor overall and disease-free survival rates. Together, these findings demonstrate that KDM4B and KDM4A promote EC progression by regulating AR activity.
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PMID:KDM4B and KDM4A promote endometrial cancer progression by regulating androgen receptor, c-myc, and p27kip1. 2639 36

Gynecological cancer is the leading cause of cancer mortality in women. However, the mechanisms underlying gynecological cancer progression have remained largely unclear. In the present study, 799 dysregulated genes were identified in ovarian serous cystadenocarcinoma (OV), 488 dysregulated genes in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC), and 621 dysregulated genes in uterine corpus endometrial carcinoma (UCEC). Bioinformatics analysis revealed that mRNA splicing and cell proliferation-associated biological processes served important roles in OV progression. Metabolism-associated biological processes played important roles in CESC progression, and protein phosphorylation and small GTPase-mediated signal transduction served important roles in UCEC progression. The present study also constructed OV, CESC and UCEC progression-associated protein-protein interaction networks to reveal the associations among these genes. Furthermore, Kaplan-Meier curve analysis showed that progression-related genes were associated with the duration of overall survival. Finally, NARS2 and TPT1 in OV, SMYD2, EGLN1, TNFRSF10D, FUT11, SYTL3, MMP8 and EREG in CESC, and SLC5A1, TXN, KDM4B, TXNDC11, HSDL2, COX16, MGAT4A, DAGLA, ELOVL7, THRB and PCOLCE2 in UCEC were identified as hub genes in cancer progression. Therefore, this study may assist in the identification of novel mechanisms underlying cancer progression and new biomarkers for gynecological cancer prognosis and therapy.
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PMID:Identification of hub genes and key pathways associated with the progression of gynecological cancer. 3178 13