Analytical and Quantitative Cytopathology and Histopathology
2020, Volume 42, Issue 1
Research Article
SNHG7 expression is upregulated in ovarian cancer and promotes cell invasion and EMT pathway
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1
Department of Obstetrics and Gynecology, General Hospital of People's Liberation Army, Beijing, China
2
Department of Obstetrics and Gynecology, Beijing Municipal Corps Hospital of Chinese People's Armed Police Force, Beijing, Beijing, China
3
Department of Obstetrics and Gynecology, China Meitan General Hospital, Beijing, Beijing, China
4
Department of Obstetrics and Gynecology, China PLA General Hospital, Beijing, China
5
Department of Medical Laboratory, China PLA General Hospital, Beijing, China
Abstract
OBJECTIVE: Long non-coding small nucleolar RNA host gene 7 (lncRNA SNHG7) has been identified as an oncogene in tumor progression. However, the role of SNHG7 in ovarian cancer remains unknown. STUDY DESIGN: The expression of circ SNHG7 was detected in human ovarian cancer tissue and adjacent normal tissue samples using quantitative reverse transcription polymerase chain reaction (qRT-PCR) analyses. The chi-squared test was used to assess the association between expression of SNHG7 and clinical pathological parameters. Cell proliferation and invasion were performed by CCK8 and transwell assays. Western blot analysis was used to detect the protein expression. RESULTS: We demonstrated that SNHG7 was significantly upregulated in human ovarian cancer tissues and cells. Higher SNHG7 expression was associated with clinical stage and lymph node metastasis. Furthermore, we demonstrated that knockdown of SNHG7 inhibited cell proliferation and cell invasion ability. Additionally, we observed that knockdown of SNHG7 suppressed the cell epithelial-mesenchymal transition (EMT) process by upregulating E-cadherin expression but downregulating MMP9 expression. CONCLUSION: These results indicated that SNHG7 expression was higher in ovarian cancer tissues and promoted cell invasion and EMT process, which may serve as a target of ovarian cancer treatment. © Science Printers and Publishers, Inc.
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