Open AccessLong non‑coding RNA CASC2 inhibits progression and predicts favorable prognosis in epithelial ovarian cancer
Author(s) -
Zhuowei Xue,
Xiaolu Zhu,
Yincheng Teng
Publication year - 2018
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2018.9550
Subject(s) - oncogene , carcinogenesis , long non coding rna , cancer research , endometrial cancer , cancer , ectopic expression , gene silencing , biology , ovarian cancer , molecular medicine , lymphovascular invasion , oncology , medicine , metastasis , cell cycle , cell culture , gene , downregulation and upregulation , biochemistry , genetics
Epithelial ovarian cancer (EOC) is one of the leading causes of cancer‑associated mortality in women. At present, the overall 5‑year survival rate of patients with EOC remains poor despite advancements in diagnosis and treatment. Long non‑coding RNAs (lncRNAs) have attracted increasing attention in recent years for their extensive roles in tumorigenesis and cancer development. The lncRNA cancer susceptibility candidate 2 (CASC2) was originally identified as a downregulated gene in endometrial cancer, and subsequent studies revealed that CASC2 was able to act as a tumor suppressor gene in various types of cancer. The present study is the first, to the best of the authors' knowledge, to identify the clinical significance and potential role of CASC2 in EOC. The results demonstrated that CASC2 was downregulated in EOC cell lines and tissues. Analysis of association between clinicopathological features and CASC2 expression levels suggested that low CASC2 expression is associated with the serous histological subtype (P<0.001), lymph node metastasis (P=0.038), poor histological grade (P<0.001) and large tumor size (P=0.001) in EOC. Furthermore, low CASC2 expression predicted poor overall survival (P<0.001) and progression‑free survival (P<0.001). Functional assays, including Cell Counting kit‑8 assays, colony formation assays, and Transwell and Matrigel assays, confirmed that silencing of CASC2 promoted the proliferation, migration and invasion of EOC cells; whereas, ectopic overexpression of CASC2 suppressed the proliferation, migration and invasion of EOC cells. In addition, in the analysis of the risk factors for poor prognosis, low CASC2 expression was identified as an independent risk factor for reduced overall survival [hazard ratio (HR)=0.417; 95% confidence interval (CI)=0.251‑0.693; P=0.001] and progression‑free survival (HR=0.426; 95% CI=0.260‑0.699; P=0.001) in patients with EOC. In conclusion, CASC2 is downregulated in EOC, and it may suppress EOC progression and is an independent risk factor for poor prognosis. CASC2 may be a promising prognostic marker and therapeutic target in EOC.