Long noncoding RNA gastric cancer‐associated transcript 3 plays oncogenic roles in glioma through sponging miR‐3127‐5p

Evidence is emerging that long noncoding RNAs (lncRNAs) play vital roles in tumorigenesis. LncRNA gastric cancer‐associated transcript 3 (GACAT3) is reported to participate in the development of breast cancer, colorectal cancer, nonsmall cell lung cancer, and gastric cancer. However, whether it is i...

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Veröffentlicht in:Journal of cellular physiology Jg. 234; H. 6; S. 8825 - 8833
Hauptverfasser: Pan, Bailin, Zhao, Ming, Xu, Longbiao
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States Wiley Subscription Services, Inc 01.06.2019
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ISSN:0021-9541, 1097-4652, 1097-4652
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Abstract Evidence is emerging that long noncoding RNAs (lncRNAs) play vital roles in tumorigenesis. LncRNA gastric cancer‐associated transcript 3 (GACAT3) is reported to participate in the development of breast cancer, colorectal cancer, nonsmall cell lung cancer, and gastric cancer. However, whether it is implicated in glioma has not been elucidated. Here, we found that GACAT3 level was aberrantly elevated in glioma tissues and cell lines. Higher GACAT3 expression predicted lower survival rate. Knockdown of GACAT3 suppressed the proliferation, colony formation, migration, and invasion but promoting apoptosis in glioma cells. Next, we determined that GACAT3 contributes to glioma progression through inhibiting microRNA (miR)‐3127‐5p. Subsequently, ELAVL1 was identified as a direct target of miR‐3127‐5p by bioinformatics analysis and luciferase reporter assay. Moreover, we confirmed that GACAT3 promoted ELAVL1 expression through sponging miR‐3127‐5p, leading to glioma progression. Taken together, our study elucidated that GACAT3/miR‐3127‐5p/ELAVL1 signaling regulates glioma development and might be a promising therapeutic target. our study elucidated that GACAT3/miR‐3127‐5p/ELAVL1 signaling regulates glioma development and might be a promising therapeutic target.
AbstractList Evidence is emerging that long noncoding RNAs (lncRNAs) play vital roles in tumorigenesis. LncRNA gastric cancer‐associated transcript 3 (GACAT3) is reported to participate in the development of breast cancer, colorectal cancer, nonsmall cell lung cancer, and gastric cancer. However, whether it is implicated in glioma has not been elucidated. Here, we found that GACAT3 level was aberrantly elevated in glioma tissues and cell lines. Higher GACAT3 expression predicted lower survival rate. Knockdown of GACAT3 suppressed the proliferation, colony formation, migration, and invasion but promoting apoptosis in glioma cells. Next, we determined that GACAT3 contributes to glioma progression through inhibiting microRNA (miR)‐3127‐5p. Subsequently, ELAVL1 was identified as a direct target of miR‐3127‐5p by bioinformatics analysis and luciferase reporter assay. Moreover, we confirmed that GACAT3 promoted ELAVL1 expression through sponging miR‐3127‐5p, leading to glioma progression. Taken together, our study elucidated that GACAT3/miR‐3127‐5p/ELAVL1 signaling regulates glioma development and might be a promising therapeutic target.
Evidence is emerging that long noncoding RNAs (lncRNAs) play vital roles in tumorigenesis. LncRNA gastric cancer-associated transcript 3 (GACAT3) is reported to participate in the development of breast cancer, colorectal cancer, nonsmall cell lung cancer, and gastric cancer. However, whether it is implicated in glioma has not been elucidated. Here, we found that GACAT3 level was aberrantly elevated in glioma tissues and cell lines. Higher GACAT3 expression predicted lower survival rate. Knockdown of GACAT3 suppressed the proliferation, colony formation, migration, and invasion but promoting apoptosis in glioma cells. Next, we determined that GACAT3 contributes to glioma progression through inhibiting microRNA (miR)-3127-5p. Subsequently, ELAVL1 was identified as a direct target of miR-3127-5p by bioinformatics analysis and luciferase reporter assay. Moreover, we confirmed that GACAT3 promoted ELAVL1 expression through sponging miR-3127-5p, leading to glioma progression. Taken together, our study elucidated that GACAT3/miR-3127-5p/ELAVL1 signaling regulates glioma development and might be a promising therapeutic target.Evidence is emerging that long noncoding RNAs (lncRNAs) play vital roles in tumorigenesis. LncRNA gastric cancer-associated transcript 3 (GACAT3) is reported to participate in the development of breast cancer, colorectal cancer, nonsmall cell lung cancer, and gastric cancer. However, whether it is implicated in glioma has not been elucidated. Here, we found that GACAT3 level was aberrantly elevated in glioma tissues and cell lines. Higher GACAT3 expression predicted lower survival rate. Knockdown of GACAT3 suppressed the proliferation, colony formation, migration, and invasion but promoting apoptosis in glioma cells. Next, we determined that GACAT3 contributes to glioma progression through inhibiting microRNA (miR)-3127-5p. Subsequently, ELAVL1 was identified as a direct target of miR-3127-5p by bioinformatics analysis and luciferase reporter assay. Moreover, we confirmed that GACAT3 promoted ELAVL1 expression through sponging miR-3127-5p, leading to glioma progression. Taken together, our study elucidated that GACAT3/miR-3127-5p/ELAVL1 signaling regulates glioma development and might be a promising therapeutic target.
Evidence is emerging that long noncoding RNAs (lncRNAs) play vital roles in tumorigenesis. LncRNA gastric cancer‐associated transcript 3 (GACAT3) is reported to participate in the development of breast cancer, colorectal cancer, nonsmall cell lung cancer, and gastric cancer. However, whether it is implicated in glioma has not been elucidated. Here, we found that GACAT3 level was aberrantly elevated in glioma tissues and cell lines. Higher GACAT3 expression predicted lower survival rate. Knockdown of GACAT3 suppressed the proliferation, colony formation, migration, and invasion but promoting apoptosis in glioma cells. Next, we determined that GACAT3 contributes to glioma progression through inhibiting microRNA (miR)‐3127‐5p. Subsequently, ELAVL1 was identified as a direct target of miR‐3127‐5p by bioinformatics analysis and luciferase reporter assay. Moreover, we confirmed that GACAT3 promoted ELAVL1 expression through sponging miR‐3127‐5p, leading to glioma progression. Taken together, our study elucidated that GACAT3/miR‐3127‐5p/ELAVL1 signaling regulates glioma development and might be a promising therapeutic target. our study elucidated that GACAT3/miR‐3127‐5p/ELAVL1 signaling regulates glioma development and might be a promising therapeutic target.
Author Zhao, Ming
Xu, Longbiao
Pan, Bailin
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Keywords long noncoding RNA
migration
glioma
invasion
proliferation
GACAT3
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Snippet Evidence is emerging that long noncoding RNAs (lncRNAs) play vital roles in tumorigenesis. LncRNA gastric cancer‐associated transcript 3 (GACAT3) is reported...
Evidence is emerging that long noncoding RNAs (lncRNAs) play vital roles in tumorigenesis. LncRNA gastric cancer-associated transcript 3 (GACAT3) is reported...
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SubjectTerms Adult
Animals
Apoptosis
Bioinformatics
Breast cancer
Cancer
Cell Movement
Cell Proliferation
Cells, Cultured
Colorectal cancer
Colorectal carcinoma
ELAV-Like Protein 1 - genetics
ELAV-Like Protein 1 - metabolism
Female
GACAT3
Gastric cancer
Gene Expression Regulation, Neoplastic - physiology
Gene Silencing
Glioma
Glioma - metabolism
Glioma cells
Humans
invasion
long noncoding RNA
Lung cancer
Male
Mice
Mice, Nude
MicroRNAs - genetics
MicroRNAs - metabolism
Middle Aged
migration
miRNA
Neoplasms, Experimental - genetics
Neoplasms, Experimental - metabolism
proliferation
Ribonucleic acid
RNA
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Survival
Target recognition
Therapeutic applications
Transcription
Tumorigenesis
Title Long noncoding RNA gastric cancer‐associated transcript 3 plays oncogenic roles in glioma through sponging miR‐3127‐5p
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjcp.27542
https://www.ncbi.nlm.nih.gov/pubmed/30317610
https://www.proquest.com/docview/2183986859
https://www.proquest.com/docview/2120205811
Volume 234
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