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Elevated expression level of long noncoding RNA MALAT-1 facilitates cell growth, migration and invasion in pancreatic cancer.
- Source :
-
Oncology reports [Oncol Rep] 2014 Dec; Vol. 32 (6), pp. 2485-92. Date of Electronic Publication: 2014 Sep 26. - Publication Year :
- 2014
-
Abstract
- Pancreatic cancer is one of the most aggressive solid malignancies with a dismal survival rate. Recent studies have shown that high expression levels of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript-1 (MALAT-1) correlate with several solid tumors. However, the underlying molecular mechanisms and its clinical significance in pancreatic cancer remain to be elucidated. In the present study, our results showed that MALAT-1 expression levels were upregulated in pancreatic cancer tissues compared with adjacent noncancerous controls. Consistently, higher expression level of MALAT-1 was found in all seven pancreatic cancer cell lines relative to the human pancreatic ductal epithelial cell. Further function analysis revealed that downregulation of MALAT-1 could inhibit tumor cell proliferation and decrease cell migration and invasion in vitro. The underlying mechanisms are possibly involved in inducing G2/M cell cycle arrest, promoting cell apoptosis, suppressing epithelial-mesenchymal transition and reducing cancer stem-like properties. In conclusion, this study indicated that MALAT-1 may serve as an oncogenic lncRNA that is involved in malignancy phenotypes of pancreatic cancer. Therefore, it may be used as a potential therapeutic target.
- Subjects :
- Apoptosis
Biomarkers, Tumor metabolism
Cell Line, Tumor
Epithelial-Mesenchymal Transition
G2 Phase Cell Cycle Checkpoints
Gene Expression
Humans
Neoplasm Invasiveness
Neoplastic Stem Cells metabolism
Pancreatic Neoplasms pathology
RNA, Long Noncoding genetics
Up-Regulation
Cell Movement
Cell Proliferation
Pancreatic Neoplasms metabolism
RNA, Long Noncoding metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1791-2431
- Volume :
- 32
- Issue :
- 6
- Database :
- MEDLINE
- Journal :
- Oncology reports
- Publication Type :
- Academic Journal
- Accession number :
- 25269958
- Full Text :
- https://doi.org/10.3892/or.2014.3518