Long non-coding RNA MEG3 functions as a tumour suppressor and has prognostic predictive value in human pancreatic cancer
Author(s) -
Ling Ma,
Feng Wang,
Chong Du,
Zhengkui Zhang,
Huahu Guo,
Xuehai Xie,
Hongqiao Gao,
Yan Zhuang,
Marko Kornmann,
Hong Gao,
Xiaodong Tian,
Yinmo Yang
Publication year - 2018
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2018.6178
Subject(s) - meg3 , oncogene , cancer research , pancreatic cancer , biology , gene knockdown , cell , cell cycle , gemcitabine , cell culture , long non coding rna , cancer , cell growth , rna , gene , genetics , biochemistry
Long non-coding RNA (lncRNA) MEG3 has been demonstrated to be a tumour suppressor in many malignancies. However, the functional role of MEG3 in pancreatic cancer (PC) is unclear. In this study, the expression pattern of MEG3 was evaluated in 25 samples of microdissected PC tissues and 8 PC cell lines and was compared to the expression in adjacent non‑cancerous tissues and a human pancreatic normal epithelial cell line. Loss of MEG3 expression was observed in both the cancerous tissues and cancer cell lines. Although the absence of expression of MEG3 was not statistically correlated to either histological grade or TNM stage in the 25 cases, the prognosis was significantly worse. MEG3 knockdown enhanced cell proliferation, promoted cell migration and invasion, induced epithelial‑mesenchymal transition (EMT), increased the sphere‑forming ability and cancer stem cell (CSC) properties, and decreased the chemosensitivity to gemcitabine in vitro. In contrast, forced expression of MEG3 resulted in a reverse effect. In conclusion, MEG3 functions as a tumour suppressor in human PC. The underlying cause of the poor prognosis induced by low levels of MEG3 expression in PC patients might involve EMT induction, enhanced CSC phenotypes and reduced chemoresistance, all of which might be associated with Snail activation.
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