IncRNA KCNQ1OTI promotes proliferation and invasion of glioma cells by targeting the miR-375/YAP pathway

The long non-coding RNA KCNQIOTI is generally recognized as an oncogenic molecule in several human malignant tumors. However, to the best of our knowledge, the role of KCNQIOTI in glioma has not been fully investigated. The current study aimed to probe the biological function of KCNQIOTI in human gl...

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Veröffentlicht in:International journal of molecular medicine 2020-12, Vol.46 (6), p.1983
Hauptverfasser: Ding, Panfeng, Liang, Bo, Shou, Jixin, Wang, Xinjun
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container_title International journal of molecular medicine
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creator Ding, Panfeng
Liang, Bo
Shou, Jixin
Wang, Xinjun
description The long non-coding RNA KCNQIOTI is generally recognized as an oncogenic molecule in several human malignant tumors. However, to the best of our knowledge, the role of KCNQIOTI in glioma has not been fully investigated. The current study aimed to probe the biological function of KCNQIOTI in human glioma cell lines and its mechanisms. The glioma cell lines U251 and U87-MG were used as cell models. Cell proliferation and apoptosis assays were used to measure the effects of different treatments on survival, and reverse transcription-quantitative PCR and western blotting were used to investigate the expression profiles of key molecules. Migration and invasion assays were conducted to reveal the biological features of glioma cells. The results indicated that KCNQIOTI was upregulated in glioma tissues compared with adjacent tissues, which was associated with poor prognosis. Additionally, knockdown of KCNQIOTI in U251 and U87-MG cells inhibited cell proliferation, migration and invasion, but had no effect on apoptosis. The effects of KCNQIOTI on migration and invasion were partially attributed to enhanced Yes-associated protein (YAP) expression levels and epithelial-mesenchymal transition (EMT) signaling. Furthermore, microRNA (miR)-375 functioned as a link between KCNQIOTI and YAP in regulating cell proliferation. Finally, the KCNQlOTl/miR-375/YAP axis modulated cell proliferation and cell fate by affecting the modulated YAP-mediated EMT signaling. In conclusion, the KCNQlOTl/miR-375/YAP axis modulated migration and invasion of glioma cells by affecting EMT signaling; thus, targeting KCNQIOTI may represent a promising strategy in glioma therapeutics.
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However, to the best of our knowledge, the role of KCNQIOTI in glioma has not been fully investigated. The current study aimed to probe the biological function of KCNQIOTI in human glioma cell lines and its mechanisms. The glioma cell lines U251 and U87-MG were used as cell models. Cell proliferation and apoptosis assays were used to measure the effects of different treatments on survival, and reverse transcription-quantitative PCR and western blotting were used to investigate the expression profiles of key molecules. Migration and invasion assays were conducted to reveal the biological features of glioma cells. The results indicated that KCNQIOTI was upregulated in glioma tissues compared with adjacent tissues, which was associated with poor prognosis. Additionally, knockdown of KCNQIOTI in U251 and U87-MG cells inhibited cell proliferation, migration and invasion, but had no effect on apoptosis. The effects of KCNQIOTI on migration and invasion were partially attributed to enhanced Yes-associated protein (YAP) expression levels and epithelial-mesenchymal transition (EMT) signaling. Furthermore, microRNA (miR)-375 functioned as a link between KCNQIOTI and YAP in regulating cell proliferation. Finally, the KCNQlOTl/miR-375/YAP axis modulated cell proliferation and cell fate by affecting the modulated YAP-mediated EMT signaling. 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source Spandidos Publications Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Analysis
Apoptosis
Gliomas
Photographic industry
RNA
Scientific equipment industry
title IncRNA KCNQ1OTI promotes proliferation and invasion of glioma cells by targeting the miR-375/YAP pathway
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