Affiliations: [a] Department of Gynecology and Obstetrics, Zhujiang Hospital,Southern Medical University, Guangzhou, Guangdong, China | [b] Department of Gynecology and Obstetrics, Hainan General Hospital, Haikou 570311, Hainan, China | [c] Department of Radiology, Hainan General Hospital, Haikou 570311, Hainan, China
Correspondence:
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Corresponding author: Yifeng Wang, Department of Gynecology and Obstetrics, Zhujiang Hospital, Southern Medical University, No. 253, Gongye Da Dao Zhong, Guangzhou 510000, Guangdong, China. Tel.: +86 20 61643888; Fax: +86 20 61643888; E-mail: yifengw1981@126.com.
Note: [1] These authors contributed equally to the work.
Abstract: BACKGROUND: Aberrant expression of long non-coding RNAs is involved in the progression of ovarian cancer. However, the clinical significance and biological functions of SNHG3 expression was little known in ovarian cancer (OC). METHODS: The SNHG3 expression in ovarian cancer tissues and paired adjacent normal tissues was detected using quantitative real time polymerase chain reaction (qRT-PCR). Gain-of function and loss-of function assays were performed in ovarian cancer cells to demonstrate the effects of SNHG3 expression on cell proliferation and invasion. The relative protein expression levels were determined using western blot analyses. RESULTS: The expression of SNHG3 was significantly up-regulated in ovarian cancer tissues compared with adjacent normal tissues. Higher SNHG3 expression levels positively associated with FIGO stage, lymph node metastasis, and poor prognosis of ovarian cancer patients. Univariate and multivariate Cox regression analysis implied that FIGO stage, lymph node metastasis, higher SNHG3 expression were independent prognostic factors for overall survival (OS) rate in ovarian cancer patients. Gain-of function and loss-of function assays demonstrated that SNHG3 knockdown inhibited ovarian cancer cell proliferation and invasion abilities. However, SNHG3 overexpression promoted ovarian cancer cell proliferation and invasion abilities. Furthermore, cell proliferation and invasion related protein CyclinD1, CDK1, MMP9 and MMP3 were significantly downregulated after SNHG3 knockdown in ovarian cancer cells, while SNHG3 overexpression had reverse effects. In addition, SNHG3 functioned as an oncogene by regulating GSK3β/β-catenin signaling activity in ovarian cancer. CONCLUSIONS: Taken together, our data provide that SNHG3 has potential clinical value of and may serve as target of ovarian cancer treatment.
Keywords: Ovarian cancer, long non-coding RNA, SNHG3, cell proliferation
