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Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis
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| Zeitschriftentitel: | Cell Proliferation |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | Cell Proliferation, 52, 2019, 5 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Chen, Yangzong Bao, Chunchun Zhang, Xiuxing Lin, Xinshi Huang, Hongou Wang, Zhiqiang Chen, Yangzong Bao, Chunchun Zhang, Xiuxing Lin, Xinshi Huang, Hongou Wang, Zhiqiang |
|---|---|
| author |
Chen, Yangzong Bao, Chunchun Zhang, Xiuxing Lin, Xinshi Huang, Hongou Wang, Zhiqiang |
| spellingShingle |
Chen, Yangzong Bao, Chunchun Zhang, Xiuxing Lin, Xinshi Huang, Hongou Wang, Zhiqiang Cell Proliferation Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis Cell Biology General Medicine |
| author_sort |
chen, yangzong |
| spelling |
Chen, Yangzong Bao, Chunchun Zhang, Xiuxing Lin, Xinshi Huang, Hongou Wang, Zhiqiang 0960-7722 1365-2184 Wiley Cell Biology General Medicine http://dx.doi.org/10.1111/cpr.12615 <jats:title>Abstract</jats:title><jats:sec><jats:title>Objectives</jats:title><jats:p>It has been widely reported that long non‐coding RNAs (lncRNAs) can participate in multiple biological processes of human cancers. lncRNA <jats:italic>HLA complex group 11 (HCG11)</jats:italic> has been reported in human cancers as a tumour suppressor. This study focused on investigating the function and mechanism of <jats:italic>HCG11</jats:italic> in glioma.</jats:p></jats:sec><jats:sec><jats:title>Materials and methods</jats:title><jats:p>Based on The Cancer Genome Atlas (TCGA) data set and qRT‐PCR analysis, the expression pattern of <jats:italic>HCG11</jats:italic> was identified in glioma samples. The mechanism associated with <jats:italic>HCG11</jats:italic> downregulation was determined by mechanism experiments. Gain‐of‐function assays were conducted for the identification of <jats:italic>HCG11</jats:italic> function in glioma progression. Mechanism investigation based on the luciferase reporter assay, RIP assay and pull‐down assay was used to explore the downstream molecular mechanism of <jats:italic>HCG11</jats:italic>. The role of molecular pathway in the progression of glioma was analysed in accordance with the rescue assays.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>HCG11</jats:italic> was expressed at low level in glioma samples compared with normal samples. FOXP1 could bind with HCG11 and transcriptionally inactivated HCG11. Overexpression of <jats:italic>HCG11</jats:italic> efficiently suppressed cell proliferation, induced cell cycle arrest and promoted cell apoptosis. <jats:italic>HCG11</jats:italic> was predominantly enriched in the cytoplasm of glioma cells and acted as a competing endogenous RNAs (ceRNAs) by sponging <jats:italic>micro‐496</jats:italic> to upregulate <jats:italic>cytoplasmic polyadenylation element binding protein 3 (CPEB3)</jats:italic>. <jats:italic>CEPB3</jats:italic> and <jats:italic>miR‐496</jats:italic> involved in <jats:italic>HCG11</jats:italic>‐mediated glioma progression.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p><jats:italic>HCG11</jats:italic> inhibited glioma progression by regulating <jats:italic>miR‐496/CPEB3</jats:italic> axis.</jats:p></jats:sec> Long non‐coding RNA <i>HCG11</i> modulates glioma progression through cooperating with <i>miR‐496/CPEB3</i> axis Cell Proliferation |
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10.1111/cpr.12615 |
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Biologie |
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Wiley, 2019 |
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Wiley, 2019 |
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0960-7722 1365-2184 |
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chen2019longnoncodingrnahcg11modulatesgliomaprogressionthroughcooperatingwithmir496cpeb3axis |
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2019 |
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Wiley |
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Cell Proliferation |
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49 |
| title |
Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis |
| title_unstemmed |
Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis |
| title_full |
Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis |
| title_fullStr |
Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis |
| title_full_unstemmed |
Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis |
| title_short |
Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis |
| title_sort |
long non‐coding rna <i>hcg11</i> modulates glioma progression through cooperating with <i>mir‐496/cpeb3</i> axis |
| topic |
Cell Biology General Medicine |
| url |
http://dx.doi.org/10.1111/cpr.12615 |
| publishDate |
2019 |
| physical |
|
| description |
<jats:title>Abstract</jats:title><jats:sec><jats:title>Objectives</jats:title><jats:p>It has been widely reported that long non‐coding RNAs (lncRNAs) can participate in multiple biological processes of human cancers. lncRNA <jats:italic>HLA complex group 11 (HCG11)</jats:italic> has been reported in human cancers as a tumour suppressor. This study focused on investigating the function and mechanism of <jats:italic>HCG11</jats:italic> in glioma.</jats:p></jats:sec><jats:sec><jats:title>Materials and methods</jats:title><jats:p>Based on The Cancer Genome Atlas (TCGA) data set and qRT‐PCR analysis, the expression pattern of <jats:italic>HCG11</jats:italic> was identified in glioma samples. The mechanism associated with <jats:italic>HCG11</jats:italic> downregulation was determined by mechanism experiments. Gain‐of‐function assays were conducted for the identification of <jats:italic>HCG11</jats:italic> function in glioma progression. Mechanism investigation based on the luciferase reporter assay, RIP assay and pull‐down assay was used to explore the downstream molecular mechanism of <jats:italic>HCG11</jats:italic>. The role of molecular pathway in the progression of glioma was analysed in accordance with the rescue assays.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>HCG11</jats:italic> was expressed at low level in glioma samples compared with normal samples. FOXP1 could bind with HCG11 and transcriptionally inactivated HCG11. Overexpression of <jats:italic>HCG11</jats:italic> efficiently suppressed cell proliferation, induced cell cycle arrest and promoted cell apoptosis. <jats:italic>HCG11</jats:italic> was predominantly enriched in the cytoplasm of glioma cells and acted as a competing endogenous RNAs (ceRNAs) by sponging <jats:italic>micro‐496</jats:italic> to upregulate <jats:italic>cytoplasmic polyadenylation element binding protein 3 (CPEB3)</jats:italic>. <jats:italic>CEPB3</jats:italic> and <jats:italic>miR‐496</jats:italic> involved in <jats:italic>HCG11</jats:italic>‐mediated glioma progression.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p><jats:italic>HCG11</jats:italic> inhibited glioma progression by regulating <jats:italic>miR‐496/CPEB3</jats:italic> axis.</jats:p></jats:sec> |
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| author | Chen, Yangzong, Bao, Chunchun, Zhang, Xiuxing, Lin, Xinshi, Huang, Hongou, Wang, Zhiqiang |
| author_facet | Chen, Yangzong, Bao, Chunchun, Zhang, Xiuxing, Lin, Xinshi, Huang, Hongou, Wang, Zhiqiang, Chen, Yangzong, Bao, Chunchun, Zhang, Xiuxing, Lin, Xinshi, Huang, Hongou, Wang, Zhiqiang |
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| description | <jats:title>Abstract</jats:title><jats:sec><jats:title>Objectives</jats:title><jats:p>It has been widely reported that long non‐coding RNAs (lncRNAs) can participate in multiple biological processes of human cancers. lncRNA <jats:italic>HLA complex group 11 (HCG11)</jats:italic> has been reported in human cancers as a tumour suppressor. This study focused on investigating the function and mechanism of <jats:italic>HCG11</jats:italic> in glioma.</jats:p></jats:sec><jats:sec><jats:title>Materials and methods</jats:title><jats:p>Based on The Cancer Genome Atlas (TCGA) data set and qRT‐PCR analysis, the expression pattern of <jats:italic>HCG11</jats:italic> was identified in glioma samples. The mechanism associated with <jats:italic>HCG11</jats:italic> downregulation was determined by mechanism experiments. Gain‐of‐function assays were conducted for the identification of <jats:italic>HCG11</jats:italic> function in glioma progression. Mechanism investigation based on the luciferase reporter assay, RIP assay and pull‐down assay was used to explore the downstream molecular mechanism of <jats:italic>HCG11</jats:italic>. The role of molecular pathway in the progression of glioma was analysed in accordance with the rescue assays.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>HCG11</jats:italic> was expressed at low level in glioma samples compared with normal samples. FOXP1 could bind with HCG11 and transcriptionally inactivated HCG11. Overexpression of <jats:italic>HCG11</jats:italic> efficiently suppressed cell proliferation, induced cell cycle arrest and promoted cell apoptosis. <jats:italic>HCG11</jats:italic> was predominantly enriched in the cytoplasm of glioma cells and acted as a competing endogenous RNAs (ceRNAs) by sponging <jats:italic>micro‐496</jats:italic> to upregulate <jats:italic>cytoplasmic polyadenylation element binding protein 3 (CPEB3)</jats:italic>. <jats:italic>CEPB3</jats:italic> and <jats:italic>miR‐496</jats:italic> involved in <jats:italic>HCG11</jats:italic>‐mediated glioma progression.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p><jats:italic>HCG11</jats:italic> inhibited glioma progression by regulating <jats:italic>miR‐496/CPEB3</jats:italic> axis.</jats:p></jats:sec> |
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| imprint | Wiley, 2019 |
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| institution | DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Rs1, DE-Pl11, DE-105, DE-14, DE-Ch1 |
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| spelling | Chen, Yangzong Bao, Chunchun Zhang, Xiuxing Lin, Xinshi Huang, Hongou Wang, Zhiqiang 0960-7722 1365-2184 Wiley Cell Biology General Medicine http://dx.doi.org/10.1111/cpr.12615 <jats:title>Abstract</jats:title><jats:sec><jats:title>Objectives</jats:title><jats:p>It has been widely reported that long non‐coding RNAs (lncRNAs) can participate in multiple biological processes of human cancers. lncRNA <jats:italic>HLA complex group 11 (HCG11)</jats:italic> has been reported in human cancers as a tumour suppressor. This study focused on investigating the function and mechanism of <jats:italic>HCG11</jats:italic> in glioma.</jats:p></jats:sec><jats:sec><jats:title>Materials and methods</jats:title><jats:p>Based on The Cancer Genome Atlas (TCGA) data set and qRT‐PCR analysis, the expression pattern of <jats:italic>HCG11</jats:italic> was identified in glioma samples. The mechanism associated with <jats:italic>HCG11</jats:italic> downregulation was determined by mechanism experiments. Gain‐of‐function assays were conducted for the identification of <jats:italic>HCG11</jats:italic> function in glioma progression. Mechanism investigation based on the luciferase reporter assay, RIP assay and pull‐down assay was used to explore the downstream molecular mechanism of <jats:italic>HCG11</jats:italic>. The role of molecular pathway in the progression of glioma was analysed in accordance with the rescue assays.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>HCG11</jats:italic> was expressed at low level in glioma samples compared with normal samples. FOXP1 could bind with HCG11 and transcriptionally inactivated HCG11. Overexpression of <jats:italic>HCG11</jats:italic> efficiently suppressed cell proliferation, induced cell cycle arrest and promoted cell apoptosis. <jats:italic>HCG11</jats:italic> was predominantly enriched in the cytoplasm of glioma cells and acted as a competing endogenous RNAs (ceRNAs) by sponging <jats:italic>micro‐496</jats:italic> to upregulate <jats:italic>cytoplasmic polyadenylation element binding protein 3 (CPEB3)</jats:italic>. <jats:italic>CEPB3</jats:italic> and <jats:italic>miR‐496</jats:italic> involved in <jats:italic>HCG11</jats:italic>‐mediated glioma progression.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p><jats:italic>HCG11</jats:italic> inhibited glioma progression by regulating <jats:italic>miR‐496/CPEB3</jats:italic> axis.</jats:p></jats:sec> Long non‐coding RNA <i>HCG11</i> modulates glioma progression through cooperating with <i>miR‐496/CPEB3</i> axis Cell Proliferation |
| spellingShingle | Chen, Yangzong, Bao, Chunchun, Zhang, Xiuxing, Lin, Xinshi, Huang, Hongou, Wang, Zhiqiang, Cell Proliferation, Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis, Cell Biology, General Medicine |
| title | Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis |
| title_full | Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis |
| title_fullStr | Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis |
| title_full_unstemmed | Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis |
| title_short | Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis |
| title_sort | long non‐coding rna <i>hcg11</i> modulates glioma progression through cooperating with <i>mir‐496/cpeb3</i> axis |
| title_unstemmed | Long non‐coding RNA HCG11 modulates glioma progression through cooperating with miR‐496/CPEB3 axis |
| topic | Cell Biology, General Medicine |
| url | http://dx.doi.org/10.1111/cpr.12615 |