Upregulated long noncoding RNA LINC01296 indicates a dismal prognosis for pancreatic ductal adenocarcinoma and promotes cell metastatic properties by affecting EMT. Issue 1 (11th September 2018)

• Record Type: Journal Article
• Authors: Yuan, Qihua; Zhang, Yuxia; Feng, Lijun; Jiang, Yuehong
• Is Part Of: Journal of cellular biochemistry. Volume 120:Issue 1(2019)
• Page Start: 552
• Page End: 561
• Publication Date: 2018-09-11
• Subjects: Epithelial‐to‐mesenchymal transition (EMT) -- LINC01296 -- long noncoding RNA (lncRNA) -- pancreatic ductal adenocarcinoma (PDAC) -- prognosis; Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.27411
• Languages: English
• ISSNs: 0730-2312

Abstract

Abstract: Background: Pancreatic ductal adenocarcinoma (PDAC) is a fatal disease that responds poorly to chemotherapy and radiotherapy and whose incidence has increased worldwide. Long noncoding RNAs have been demonstrated to play important roles in cancer initiation and progression. Long intergenic non‐coding RNA 01296 (LINC01296) has been reported to be upregulated in several malignancies, but the clinical relevance and biological role of LINC01296 in PDAC are still unclear. Methods: RT‐qPCR was performed to evaluate the expression of LINC01296 in 85 pared PDAC tissue samples and a panel of PDAC cell lines. The clinical value and prognostic role of LINC01296 in patients with PDAC were further explored. Furthermore, we explored the functional roles of LINC01296 depletion in PANC‐1 and SW1990 cells, including cell proliferation, apoptosis, migration, invasion, and epithelial‐to‐mesenchymal transition (EMT). Results: LINC01296 was enhanced in PDAC tissues and cell lines, and this overexpression was correlated with advanced tumor stages and positive lymph node metastasis in patients with PDAC. In addition, upregulation of LINC01296 was an independent prognostic predictor for patients with PDAC after surgery. Moreover, silencing of LINC01296 followed by treatment with small interfering RNAs suppressed cell proliferation and promoted cell apoptosis by affecting the Bcl‐2/caspase‐3 pathway. Importantly, LINC01296 attenuation impaired the migratory and invasive potential partly by reversing EMT. Conclusions: Overall, our work may help to develop a novel prognostic biomarker and therapeutic target for PDAC. Abstract : Upregulated LINC01296 is associated with advanced tumor stage, positive lymph node invasion, and poorer prognosis in patients with pancreatic ductal adenocarcinoma. LINC01296 protects against cell apoptosis partly by affecting the Bcl‐2/caspase‐3 pathway. Silenced LINC01296 impaired metastatic properties partly by reversing epithelial‐to‐mesenchymal transition.