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Title:
Downregulation of lncRNA-MALAT1 Affects Proliferation and the Expression of Stemness Markers in Glioma Stem Cell Line SHG139S | Cellular and Molecular Neurobiology
Description:
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.
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pubmed, article, google, scholar, cas, cancer, noncoding, cell, central, rna, stem, malat, cells, long, zhang, glioma, wang, zhou, proliferation, research, expression, downregulation, huang, metastasis, chen, shgs, human, gene, access, rnas, yang, privacy, cookies, content, molecular, stemness, line, sun, erkmapk, res, liu, nature, biol, mol, author, information, journal, publish, search, markers,
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activate erk/mapk signaling month download article/chapter erk/mapk pathway youxin zhouĀ &Ā ziwei du high-grade malignant glioma glioblastoma stem cells cell-penetrating peptide based anti-apoptotic protein g1p3 lncrna-malat1 affects proliferation inducing epithelial-mesenchymal transition glioma stem cells long nuclear-retained full article pdf mesenchymal stem cells including gastric cancer human tumor growth related subjects neck cancer stem long noncoding rna large noncoding rna long noncoding rnas sc35 splicing domains privacy choices/manage cookies nuclear transcripts identifies coding rna point gallbladder cancer cells noncoding rna mapping noncoding rna anril meg3 noncoding rna molecular profiles linked noncoding rnas article cellular article han nerve research laboratory stem cells activate ltbp3 gene modulating gene expression expression profile glioma cells check access montoya-burgos ji promote cancer metastasis colorectal cancer metastasis instant access yulun huang molecular neurobiology aims european economic area de bakker pi encode pilot project isolated spiral galaxy
Questions {ā}
- Chen LL, Carmichael GG (2010) Long noncoding RNAs in mammalian cells: what, where, and why?
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headline:Downregulation of lncRNA-MALAT1 Affects Proliferation and the Expression of Stemness Markers in Glioma Stem Cell Line SHG139S
description: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.
datePublished:2015-12-09T00:00:00Z
dateModified:2015-12-09T00:00:00Z
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sameAs:https://doi.org/10.1007/s10571-015-0303-6
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Glioma
lncRNA
MALAT1
ERK/MAPK
Neurosciences
Cell Biology
Neurobiology
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headline:Downregulation of lncRNA-MALAT1 Affects Proliferation and the Expression of Stemness Markers in Glioma Stem Cell Line SHG139S
description: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.
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Glioma
lncRNA
MALAT1
ERK/MAPK
Neurosciences
Cell Biology
Neurobiology
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umbower%2CH&author=Clawson%2CH&author=Hillman-Jackson%2CJ&author=Zweig%2CAS&author=Smith%2CK&author=Thakkapallayil%2CA&author=Barber%2CG&author=Kuhn%2CRM&author=Karolchik%2CD&author=Armengol%2CL&author=Bird%2CCP&author=Bakker%2CPI&author=Kern%2CAD&author=Lopez-Bigas%2CN&author=Martin%2CJD&author=Stranger%2CBE&author=Woodroffe%2CA&author=Davydov%2CE&author=Dimas%2CA&author=Eyras%2CE&author=Hallgrimsdottir%2CIB&author=Huppert%2CJ&author=Zody%2CMC&author=Abecasis%2CGR&author=Estivill%2CX&author=Bouffard%2CGG&author=Guan%2CX&author=Hansen%2CNF&author=Idol%2CJR&author=Maduro%2CVV&author=Maskeri%2CB&author=McDowell%2CJC&author=Park%2CM&author=Thomas%2CPJ&author=Young%2CAC&author=Blakesley%2CRW&author=Muzny%2CDM&author=Sodergren%2CE&author=Wheeler%2CDA&author=Worley%2CKC&author=Jiang%2CH&author=Weinstock%2CGM&author=Gibbs%2CRA&author=Graves%2CT&author=Fulton%2CR&author=Mardis%2CER&author=Wilson%2CRK&author=Clamp%2CM&author=Cuff%2CJ&author=Gnerre%2CS&author=Jaffe%2CDB&author=Chang%2CJL&author=Lindblad-Toh%2CK&author=Lander%2CES&author=Koriabine%2CM&author=Nefedov%2CM&author=Osoegawa%2CK&author=Yoshinaga%2CY&author=Zhu%2CB&author=Jong%2CPJ
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