MicroRNA-383-5p inhibits the progression of gastric carcinoma via targeting HDAC9 expression
MicroRNAs (miRNAs), as post-transcriptional regulators, have been reported to be involved in the initiation and progression of various types of cancer, including gastric cancer (GC). The present study aimed to investigate the role of miR-383-5p in gastric carcinogenesis. Cell viability was analyzed...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Gang Xu [verfasserIn] Na Li [verfasserIn] Yan Zhang [verfasserIn] Jinbiao Zhang [verfasserIn] Rui Xu [verfasserIn] Yanling Wu [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Schlagwörter: |
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| Übergeordnetes Werk: |
In: Brazilian Journal of Medical and Biological Research - Associação Brasileira de Divulgação Científica, 2004 |
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| Links: |
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| DOI / URN: |
10.1590/1414-431x20198341 |
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| Katalog-ID: |
DOAJ01898469X |
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| 520 | |a MicroRNAs (miRNAs), as post-transcriptional regulators, have been reported to be involved in the initiation and progression of various types of cancer, including gastric cancer (GC). The present study aimed to investigate the role of miR-383-5p in gastric carcinogenesis. Cell viability was analyzed using CCK-8 kit. Annexin V-fluorescein isothiocyanate/propidium iodide double staining was used to evaluate cell apoptosis. The expression levels of miR-383-5p and histone deacetylase 9 (HDAC9) mRNA in GC tissues and cell lines were analyzed using RT-qPCR. The protein expression of HDAC9 was detected by western blotting. We found that HDAC9 was up-regulated and miR-383-5p was down-regulated in GC tissues and cell lines. High HDAC9 expression or low miR-383-5p expression was closely related to poor prognosis and metastasis in GC patients. HDAC9 knockout or miR-383-5p mimics led to growth inhibition and increased apoptosis in AGS and SGC-7901 cells. More importantly, we validated that miR-383-5p as a post-transcriptional regulator inhibited HDAC9 expression and was inversely correlated with HDAC9 expression in GC tissues. miR-383-5p had the opposite effects to HDAC9 in gastric carcinogenesis. miR-383-5p played an important role in gastric carcinogenesis, and it is one of the important mechanisms to regulate oncogenic HDAC9 in GC, which might be helpful in the development of novel therapeutic strategies for the treatment of GC. | ||
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10.1590/1414-431x20198341 doi (DE-627)DOAJ01898469X (DE-599)DOAJa1c568e3c35842fba344d19013785d3a DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Gang Xu verfasserin aut MicroRNA-383-5p inhibits the progression of gastric carcinoma via targeting HDAC9 expression Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier MicroRNAs (miRNAs), as post-transcriptional regulators, have been reported to be involved in the initiation and progression of various types of cancer, including gastric cancer (GC). The present study aimed to investigate the role of miR-383-5p in gastric carcinogenesis. Cell viability was analyzed using CCK-8 kit. Annexin V-fluorescein isothiocyanate/propidium iodide double staining was used to evaluate cell apoptosis. The expression levels of miR-383-5p and histone deacetylase 9 (HDAC9) mRNA in GC tissues and cell lines were analyzed using RT-qPCR. The protein expression of HDAC9 was detected by western blotting. We found that HDAC9 was up-regulated and miR-383-5p was down-regulated in GC tissues and cell lines. High HDAC9 expression or low miR-383-5p expression was closely related to poor prognosis and metastasis in GC patients. HDAC9 knockout or miR-383-5p mimics led to growth inhibition and increased apoptosis in AGS and SGC-7901 cells. More importantly, we validated that miR-383-5p as a post-transcriptional regulator inhibited HDAC9 expression and was inversely correlated with HDAC9 expression in GC tissues. miR-383-5p had the opposite effects to HDAC9 in gastric carcinogenesis. miR-383-5p played an important role in gastric carcinogenesis, and it is one of the important mechanisms to regulate oncogenic HDAC9 in GC, which might be helpful in the development of novel therapeutic strategies for the treatment of GC. MicroRNA-383-5p Gastric cancer HDAC9 Post-transcriptional regulation Medicine (General) Biology (General) Na Li verfasserin aut Yan Zhang verfasserin aut Jinbiao Zhang verfasserin aut Rui Xu verfasserin aut Yanling Wu verfasserin aut In Brazilian Journal of Medical and Biological Research Associação Brasileira de Divulgação Científica, 2004 (DE-627)324613407 (DE-600)2028749-5 1414431X nnns https://doi.org/10.1590/1414-431x20198341 kostenfrei https://doaj.org/article/a1c568e3c35842fba344d19013785d3a kostenfrei http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2019000800602&lng=en&tlng=en kostenfrei https://doaj.org/toc/1414-431X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA AR |
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10.1590/1414-431x20198341 doi (DE-627)DOAJ01898469X (DE-599)DOAJa1c568e3c35842fba344d19013785d3a DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Gang Xu verfasserin aut MicroRNA-383-5p inhibits the progression of gastric carcinoma via targeting HDAC9 expression Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier MicroRNAs (miRNAs), as post-transcriptional regulators, have been reported to be involved in the initiation and progression of various types of cancer, including gastric cancer (GC). The present study aimed to investigate the role of miR-383-5p in gastric carcinogenesis. Cell viability was analyzed using CCK-8 kit. Annexin V-fluorescein isothiocyanate/propidium iodide double staining was used to evaluate cell apoptosis. The expression levels of miR-383-5p and histone deacetylase 9 (HDAC9) mRNA in GC tissues and cell lines were analyzed using RT-qPCR. The protein expression of HDAC9 was detected by western blotting. We found that HDAC9 was up-regulated and miR-383-5p was down-regulated in GC tissues and cell lines. High HDAC9 expression or low miR-383-5p expression was closely related to poor prognosis and metastasis in GC patients. HDAC9 knockout or miR-383-5p mimics led to growth inhibition and increased apoptosis in AGS and SGC-7901 cells. More importantly, we validated that miR-383-5p as a post-transcriptional regulator inhibited HDAC9 expression and was inversely correlated with HDAC9 expression in GC tissues. miR-383-5p had the opposite effects to HDAC9 in gastric carcinogenesis. miR-383-5p played an important role in gastric carcinogenesis, and it is one of the important mechanisms to regulate oncogenic HDAC9 in GC, which might be helpful in the development of novel therapeutic strategies for the treatment of GC. MicroRNA-383-5p Gastric cancer HDAC9 Post-transcriptional regulation Medicine (General) Biology (General) Na Li verfasserin aut Yan Zhang verfasserin aut Jinbiao Zhang verfasserin aut Rui Xu verfasserin aut Yanling Wu verfasserin aut In Brazilian Journal of Medical and Biological Research Associação Brasileira de Divulgação Científica, 2004 (DE-627)324613407 (DE-600)2028749-5 1414431X nnns https://doi.org/10.1590/1414-431x20198341 kostenfrei https://doaj.org/article/a1c568e3c35842fba344d19013785d3a kostenfrei http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2019000800602&lng=en&tlng=en kostenfrei https://doaj.org/toc/1414-431X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA AR |
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MicroRNA-383-5p inhibits the progression of gastric carcinoma via targeting HDAC9 expression |
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MicroRNA-383-5p inhibits the progression of gastric carcinoma via targeting HDAC9 expression |
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Gang Xu |
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Brazilian Journal of Medical and Biological Research |
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MicroRNA-383-5p inhibits the progression of gastric carcinoma via targeting HDAC9 expression |
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MicroRNAs (miRNAs), as post-transcriptional regulators, have been reported to be involved in the initiation and progression of various types of cancer, including gastric cancer (GC). The present study aimed to investigate the role of miR-383-5p in gastric carcinogenesis. Cell viability was analyzed using CCK-8 kit. Annexin V-fluorescein isothiocyanate/propidium iodide double staining was used to evaluate cell apoptosis. The expression levels of miR-383-5p and histone deacetylase 9 (HDAC9) mRNA in GC tissues and cell lines were analyzed using RT-qPCR. The protein expression of HDAC9 was detected by western blotting. We found that HDAC9 was up-regulated and miR-383-5p was down-regulated in GC tissues and cell lines. High HDAC9 expression or low miR-383-5p expression was closely related to poor prognosis and metastasis in GC patients. HDAC9 knockout or miR-383-5p mimics led to growth inhibition and increased apoptosis in AGS and SGC-7901 cells. More importantly, we validated that miR-383-5p as a post-transcriptional regulator inhibited HDAC9 expression and was inversely correlated with HDAC9 expression in GC tissues. miR-383-5p had the opposite effects to HDAC9 in gastric carcinogenesis. miR-383-5p played an important role in gastric carcinogenesis, and it is one of the important mechanisms to regulate oncogenic HDAC9 in GC, which might be helpful in the development of novel therapeutic strategies for the treatment of GC. |
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MicroRNAs (miRNAs), as post-transcriptional regulators, have been reported to be involved in the initiation and progression of various types of cancer, including gastric cancer (GC). The present study aimed to investigate the role of miR-383-5p in gastric carcinogenesis. Cell viability was analyzed using CCK-8 kit. Annexin V-fluorescein isothiocyanate/propidium iodide double staining was used to evaluate cell apoptosis. The expression levels of miR-383-5p and histone deacetylase 9 (HDAC9) mRNA in GC tissues and cell lines were analyzed using RT-qPCR. The protein expression of HDAC9 was detected by western blotting. We found that HDAC9 was up-regulated and miR-383-5p was down-regulated in GC tissues and cell lines. High HDAC9 expression or low miR-383-5p expression was closely related to poor prognosis and metastasis in GC patients. HDAC9 knockout or miR-383-5p mimics led to growth inhibition and increased apoptosis in AGS and SGC-7901 cells. More importantly, we validated that miR-383-5p as a post-transcriptional regulator inhibited HDAC9 expression and was inversely correlated with HDAC9 expression in GC tissues. miR-383-5p had the opposite effects to HDAC9 in gastric carcinogenesis. miR-383-5p played an important role in gastric carcinogenesis, and it is one of the important mechanisms to regulate oncogenic HDAC9 in GC, which might be helpful in the development of novel therapeutic strategies for the treatment of GC. |
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MicroRNAs (miRNAs), as post-transcriptional regulators, have been reported to be involved in the initiation and progression of various types of cancer, including gastric cancer (GC). The present study aimed to investigate the role of miR-383-5p in gastric carcinogenesis. Cell viability was analyzed using CCK-8 kit. Annexin V-fluorescein isothiocyanate/propidium iodide double staining was used to evaluate cell apoptosis. The expression levels of miR-383-5p and histone deacetylase 9 (HDAC9) mRNA in GC tissues and cell lines were analyzed using RT-qPCR. The protein expression of HDAC9 was detected by western blotting. We found that HDAC9 was up-regulated and miR-383-5p was down-regulated in GC tissues and cell lines. High HDAC9 expression or low miR-383-5p expression was closely related to poor prognosis and metastasis in GC patients. HDAC9 knockout or miR-383-5p mimics led to growth inhibition and increased apoptosis in AGS and SGC-7901 cells. More importantly, we validated that miR-383-5p as a post-transcriptional regulator inhibited HDAC9 expression and was inversely correlated with HDAC9 expression in GC tissues. miR-383-5p had the opposite effects to HDAC9 in gastric carcinogenesis. miR-383-5p played an important role in gastric carcinogenesis, and it is one of the important mechanisms to regulate oncogenic HDAC9 in GC, which might be helpful in the development of novel therapeutic strategies for the treatment of GC. |
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MicroRNA-383-5p inhibits the progression of gastric carcinoma via targeting HDAC9 expression |
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