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Downregulation of lncRNA-MALAT1 Affects Proliferation and the Expression of Stemness Markers in Glioma Stem Cell Line SHG139S.
- Source :
-
Cellular and molecular neurobiology [Cell Mol Neurobiol] 2016 Oct; Vol. 36 (7), pp. 1097-107. Date of Electronic Publication: 2015 Dec 09. - Publication Year :
- 2016
-
Abstract
- Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is among the most abundant and highly conserved lncRNAs, which has been detected in a wide variety of human tumors, including gastric cancer, gallbladder cancer, and so on. Previous research has showed that MALAT1 can activate LTBP3 gene in mesenchymal stem cells. However, the specific roles of MALAT1 in glioma stem cells (GSCs) remain unclear. In this study, we aimed to identify the effects of MALAT1 on proliferation and the expression of stemness markers on glioma stem cell line SHG139S. Our results showed that downregulation of MALAT1 suppressed the expression of Sox2 and Nestin which are related to stemness, while downregulation of MALAT1 promoted the proliferation in SHG139S. Further research on the underlying mechanism showed that the effects of MALAT1 downregulation on SHG139S were through regulating ERK/MAPk signaling activity. And we also found that downregulation of MALAT1 could activate ERK/MAPK signaling and promoted proliferation in SHG139 cells. These findings show that MALAT1 plays an important role in regulating the expression of stemness markers and proliferation of SHG139S, and provide a new research direction to target the progression of GSCs.
- Subjects :
- Brain Neoplasms pathology
Cell Line, Tumor
Down-Regulation
Glioma pathology
Humans
Brain Neoplasms metabolism
Cell Proliferation physiology
Gene Expression Regulation, Neoplastic
Glioma metabolism
Mesenchymal Stem Cells metabolism
Neoplastic Stem Cells metabolism
RNA, Long Noncoding genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1573-6830
- Volume :
- 36
- Issue :
- 7
- Database :
- MEDLINE
- Journal :
- Cellular and molecular neurobiology
- Publication Type :
- Academic Journal
- Accession number :
- 26649728
- Full Text :
- https://doi.org/10.1007/s10571-015-0303-6