학술논문

Knockdown of enhancer of rudimentary homolog inhibits proliferation and metastasis in ovarian cancer by regulating epithelial-mesenchymal transition
Document Type
article
Source
Biomedicine & Pharmacotherapy, Vol 125, Iss , Pp 109974- (2020)
Subject
Ovarian cancer
Proliferation
Nhancer of rudimentary homolog (ERH)
Epithelial-mesenchymal transition (EMT)
Therapeutics. Pharmacology
RM1-950
Language
English
ISSN
0753-3322
Abstract
Ovarian cancer (OC) is the deadliest gynecological malignancy. The pathogenesis of molecular in epithelial ovarian cancer (EOC), main histological type of OC, has not been completely defined. Enhancer of rudimentary homolog (ERH) had been reported to participate in transcriptional regulation, mRNA splicing, DNA repair and DNA synthesis by binding a variety of proteins. In this study, immunohistochemical staining revealed that the protein expression of ERH was associated with histological type, lymph node metastasis and pathological grade in EOC patients. To verify the association of ERH with the prognosis of OC, a GSE microarray dataset was downloaded from the Gene Expression Omnibus (GEO) database. Survival analysis suggested that ERH may be associated with poor prognosis of OC. In addition, shRNA was used to knockdown the protein and mRNA expression levels of ERH in the OC cell line SKOV3. Inhibition of ERH expression slowed proliferation, promoted apoptosis and inhibited metastasis and invasion by regulating epithelial-mesenchymal transition (EMT) in SKOV3 cells. These results indicate that ERH protein promotes the development of OC and provides an experimental basis for ERH as the potential target for ovarian cancer treatment.