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Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma
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Zeitschriftentitel: | Journal of Cellular Physiology |
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Personen und Körperschaften: | , , , , , , , |
In: | Journal of Cellular Physiology, 235, 2020, 4, S. 3835-3848 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Wiley
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Schlagwörter: |
author_facet |
Tang, Chuanxi Wang, Yue Zhang, Lei Wang, Jie Wang, Wei Han, Xiao Mu, Chunyan Gao, Dianshuai Tang, Chuanxi Wang, Yue Zhang, Lei Wang, Jie Wang, Wei Han, Xiao Mu, Chunyan Gao, Dianshuai |
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author |
Tang, Chuanxi Wang, Yue Zhang, Lei Wang, Jie Wang, Wei Han, Xiao Mu, Chunyan Gao, Dianshuai |
spellingShingle |
Tang, Chuanxi Wang, Yue Zhang, Lei Wang, Jie Wang, Wei Han, Xiao Mu, Chunyan Gao, Dianshuai Journal of Cellular Physiology Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma Cell Biology Clinical Biochemistry Physiology |
author_sort |
tang, chuanxi |
spelling |
Tang, Chuanxi Wang, Yue Zhang, Lei Wang, Jie Wang, Wei Han, Xiao Mu, Chunyan Gao, Dianshuai 0021-9541 1097-4652 Wiley Cell Biology Clinical Biochemistry Physiology http://dx.doi.org/10.1002/jcp.29278 <jats:title>Abstract</jats:title><jats:p>Glioblastoma multiforme (GBM) is a highly proliferative cancer with generally poor prognosis and accumulating evidence has highlighted the potential of long noncoding RNAs (lncRNAs) in the biological behaviors of glioma cells. This study focused on the identification of lncRNAs to identify targets for possible GBM prognosis. Microarray expression profiling found that 1,759 lncRNAs and 3,026 messenger RNAs (mRNAs) were upregulated, and 1932s lncRNA and 2,979 mRNAs were downregulated in GBM. Bioinformatics analysis and experimental verification identified TCONS_00020456 (TCON) for further analysis. In situ hybridization, along with immunohistochemical and receiver operating characteristic analysis determined TCON (truncation value = 3.5) as highly sensitive and specific in GBM. Grade IV patients with glioma life span with different lncRNA staining scores were analyzed. TCON staining scores below 3.5 indicated poor prognosis (life span ranging from 0.25 to 7 months), even if the glioma was surgically removed. TCON decreased significantly in GBM, and showed a coexpressional relationship with Smad2 and protein kinase C α (PKCα). Overexpression of TCON reduced the proliferation on one hand and migration, invasion on the other. TCON also inhibited epithelial–mesenchymal transformation and glioma progression in vivo, based on a nude mouse tumorigenicity assay. In addition, we predicted a potential binding site and intersection that microRNAs targeting Smad2, PKCα, and TCON through RACE pretest and bioinformatics analysis. Taken together, TCON, regarded as oncosuppressor, targeting the Smad2/PKCα axis plays a novel role in inhibiting the malignant progression of glioma. Moreover, it also demonstrates that the level of TCON can be used as a prognostic and diagnostic biomarker for GBM.</jats:p> Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma Journal of Cellular Physiology |
doi_str_mv |
10.1002/jcp.29278 |
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Biologie Medizin Chemie und Pharmazie |
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2020 |
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Wiley |
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Journal of Cellular Physiology |
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title |
Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma |
title_unstemmed |
Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma |
title_full |
Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma |
title_fullStr |
Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma |
title_full_unstemmed |
Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma |
title_short |
Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma |
title_sort |
identification of novel lncrna targeting smad2/pkcα signal pathway to negatively regulate malignant progression of glioblastoma |
topic |
Cell Biology Clinical Biochemistry Physiology |
url |
http://dx.doi.org/10.1002/jcp.29278 |
publishDate |
2020 |
physical |
3835-3848 |
description |
<jats:title>Abstract</jats:title><jats:p>Glioblastoma multiforme (GBM) is a highly proliferative cancer with generally poor prognosis and accumulating evidence has highlighted the potential of long noncoding RNAs (lncRNAs) in the biological behaviors of glioma cells. This study focused on the identification of lncRNAs to identify targets for possible GBM prognosis. Microarray expression profiling found that 1,759 lncRNAs and 3,026 messenger RNAs (mRNAs) were upregulated, and 1932s lncRNA and 2,979 mRNAs were downregulated in GBM. Bioinformatics analysis and experimental verification identified TCONS_00020456 (TCON) for further analysis. In situ hybridization, along with immunohistochemical and receiver operating characteristic analysis determined TCON (truncation value = 3.5) as highly sensitive and specific in GBM. Grade IV patients with glioma life span with different lncRNA staining scores were analyzed. TCON staining scores below 3.5 indicated poor prognosis (life span ranging from 0.25 to 7 months), even if the glioma was surgically removed. TCON decreased significantly in GBM, and showed a coexpressional relationship with Smad2 and protein kinase C α (PKCα). Overexpression of TCON reduced the proliferation on one hand and migration, invasion on the other. TCON also inhibited epithelial–mesenchymal transformation and glioma progression in vivo, based on a nude mouse tumorigenicity assay. In addition, we predicted a potential binding site and intersection that microRNAs targeting Smad2, PKCα, and TCON through RACE pretest and bioinformatics analysis. Taken together, TCON, regarded as oncosuppressor, targeting the Smad2/PKCα axis plays a novel role in inhibiting the malignant progression of glioma. Moreover, it also demonstrates that the level of TCON can be used as a prognostic and diagnostic biomarker for GBM.</jats:p> |
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author | Tang, Chuanxi, Wang, Yue, Zhang, Lei, Wang, Jie, Wang, Wei, Han, Xiao, Mu, Chunyan, Gao, Dianshuai |
author_facet | Tang, Chuanxi, Wang, Yue, Zhang, Lei, Wang, Jie, Wang, Wei, Han, Xiao, Mu, Chunyan, Gao, Dianshuai, Tang, Chuanxi, Wang, Yue, Zhang, Lei, Wang, Jie, Wang, Wei, Han, Xiao, Mu, Chunyan, Gao, Dianshuai |
author_sort | tang, chuanxi |
container_issue | 4 |
container_start_page | 3835 |
container_title | Journal of Cellular Physiology |
container_volume | 235 |
description | <jats:title>Abstract</jats:title><jats:p>Glioblastoma multiforme (GBM) is a highly proliferative cancer with generally poor prognosis and accumulating evidence has highlighted the potential of long noncoding RNAs (lncRNAs) in the biological behaviors of glioma cells. This study focused on the identification of lncRNAs to identify targets for possible GBM prognosis. Microarray expression profiling found that 1,759 lncRNAs and 3,026 messenger RNAs (mRNAs) were upregulated, and 1932s lncRNA and 2,979 mRNAs were downregulated in GBM. Bioinformatics analysis and experimental verification identified TCONS_00020456 (TCON) for further analysis. In situ hybridization, along with immunohistochemical and receiver operating characteristic analysis determined TCON (truncation value = 3.5) as highly sensitive and specific in GBM. Grade IV patients with glioma life span with different lncRNA staining scores were analyzed. TCON staining scores below 3.5 indicated poor prognosis (life span ranging from 0.25 to 7 months), even if the glioma was surgically removed. TCON decreased significantly in GBM, and showed a coexpressional relationship with Smad2 and protein kinase C α (PKCα). Overexpression of TCON reduced the proliferation on one hand and migration, invasion on the other. TCON also inhibited epithelial–mesenchymal transformation and glioma progression in vivo, based on a nude mouse tumorigenicity assay. In addition, we predicted a potential binding site and intersection that microRNAs targeting Smad2, PKCα, and TCON through RACE pretest and bioinformatics analysis. Taken together, TCON, regarded as oncosuppressor, targeting the Smad2/PKCα axis plays a novel role in inhibiting the malignant progression of glioma. Moreover, it also demonstrates that the level of TCON can be used as a prognostic and diagnostic biomarker for GBM.</jats:p> |
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spelling | Tang, Chuanxi Wang, Yue Zhang, Lei Wang, Jie Wang, Wei Han, Xiao Mu, Chunyan Gao, Dianshuai 0021-9541 1097-4652 Wiley Cell Biology Clinical Biochemistry Physiology http://dx.doi.org/10.1002/jcp.29278 <jats:title>Abstract</jats:title><jats:p>Glioblastoma multiforme (GBM) is a highly proliferative cancer with generally poor prognosis and accumulating evidence has highlighted the potential of long noncoding RNAs (lncRNAs) in the biological behaviors of glioma cells. This study focused on the identification of lncRNAs to identify targets for possible GBM prognosis. Microarray expression profiling found that 1,759 lncRNAs and 3,026 messenger RNAs (mRNAs) were upregulated, and 1932s lncRNA and 2,979 mRNAs were downregulated in GBM. Bioinformatics analysis and experimental verification identified TCONS_00020456 (TCON) for further analysis. In situ hybridization, along with immunohistochemical and receiver operating characteristic analysis determined TCON (truncation value = 3.5) as highly sensitive and specific in GBM. Grade IV patients with glioma life span with different lncRNA staining scores were analyzed. TCON staining scores below 3.5 indicated poor prognosis (life span ranging from 0.25 to 7 months), even if the glioma was surgically removed. TCON decreased significantly in GBM, and showed a coexpressional relationship with Smad2 and protein kinase C α (PKCα). Overexpression of TCON reduced the proliferation on one hand and migration, invasion on the other. TCON also inhibited epithelial–mesenchymal transformation and glioma progression in vivo, based on a nude mouse tumorigenicity assay. In addition, we predicted a potential binding site and intersection that microRNAs targeting Smad2, PKCα, and TCON through RACE pretest and bioinformatics analysis. Taken together, TCON, regarded as oncosuppressor, targeting the Smad2/PKCα axis plays a novel role in inhibiting the malignant progression of glioma. Moreover, it also demonstrates that the level of TCON can be used as a prognostic and diagnostic biomarker for GBM.</jats:p> Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma Journal of Cellular Physiology |
spellingShingle | Tang, Chuanxi, Wang, Yue, Zhang, Lei, Wang, Jie, Wang, Wei, Han, Xiao, Mu, Chunyan, Gao, Dianshuai, Journal of Cellular Physiology, Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma, Cell Biology, Clinical Biochemistry, Physiology |
title | Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma |
title_full | Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma |
title_fullStr | Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma |
title_full_unstemmed | Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma |
title_short | Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma |
title_sort | identification of novel lncrna targeting smad2/pkcα signal pathway to negatively regulate malignant progression of glioblastoma |
title_unstemmed | Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma |
topic | Cell Biology, Clinical Biochemistry, Physiology |
url | http://dx.doi.org/10.1002/jcp.29278 |