Open AccessH19 promotes endometrial cancer progression by modulating epithelial-mesenchymal transition
Author(s) -
Le Zhao,
Zhen Li,
Wei Chen,
Wentao Zhai,
Jingjing Pan,
Huan Pang,
Li Xu
Publication year - 2016
Publication title -
oncology letters
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2016.5389
Subject(s) - endometrial cancer , epithelial–mesenchymal transition , oncogene , cancer research , vimentin , cancer , gene knockdown , biology , downregulation and upregulation , cell cycle , bladder cancer , molecular medicine , malignancy , small interfering rna , metastasis , oncology , medicine , transfection , cell culture , immunohistochemistry , gene , biochemistry , genetics
Endometrial cancer is one of the most common types of gynecological malignancy worldwide. Novel biomarkers and therapeutic targets are imperative for improving patients' survival. Previous studies have suggested the long non-coding RNA H19 as a potential cancer biomarker. To investigate the role of H19 in endometrial cancer, the present study examined the expression pattern of H19 in endometrial cancer tissues by quantitative polymerase chain reaction, and characterized its function in the endometrial cancer cell line via knocking down its expression with small interfering RNAs. It was found that H19 level was significantly higher in tumor tissues than in paratumoral tissues. Knockdown of H19 did not affect the growth rate of HEC-1-B endometrial cancer cells, but significantly suppressed in vitro migration and invasion of HEC-1-B cells. Furthermore, H19 downregulation decreased Snail level and increased E-cadherin expression without affecting vimentin level, indicating partial reversion of epithelial-mesenchymal transition (EMT). The present findings suggested that H19 contributed to the aggressiveness of endometrial cancer by modulating EMT process.