Silencing HOXD10 by promoter region hypermethylation activates ERK signaling in hepatocellular carcinoma
Abstract Background Hepatocellular carcinoma is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. Dysregulation of HomeoboxD10 (HOXD10) was found to suppress or promote cancer progression in different cancer types. The function and regulation of HOXD10 r...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Yulin Guo [verfasserIn] Yaojun Peng [verfasserIn] Dan Gao [verfasserIn] Meiying Zhang [verfasserIn] Weili Yang [verfasserIn] Enqiang Linghu [verfasserIn] James G. Herman [verfasserIn] François Fuks [verfasserIn] Guanglong Dong [verfasserIn] Mingzhou Guo [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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In: Clinical Epigenetics ; 9(2017), 1, Seite 13 volume:9 ; year:2017 ; number:1 ; pages:13 |
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Link aufrufen |
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| DOI / URN: |
10.1186/s13148-017-0412-9 |
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| Katalog-ID: |
DOAJ077508769 |
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| 520 | |a Abstract Background Hepatocellular carcinoma is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. Dysregulation of HomeoboxD10 (HOXD10) was found to suppress or promote cancer progression in different cancer types. The function and regulation of HOXD10 remain unclear in human hepatocellular carcinoma (HCC). Methods Primary HCC samples (117), normal liver tissue samples (15), and 13 HCC cell lines (SNU182, SNU449, HBXF344, SMMC7721, Huh7, HepG2, LM3, PLC/PRF/5, BEL7402, SNU387, SNU475, QGY7703, and Huh1) were included in this study. Methylation-specific PCR, flow cytometry, western blot, transwell, siRNA, and chromatin immunoprecipitation assays were employed. Results HOXD10 was methylated in 76.9% (90/117) of human primary HCC samples. HOXD10 methylation was significantly associated with vessel cancerous embolus, tumor cell differentiation, and the 3-year overall survival rate (all P < 0.05). The expression of HOXD10 was regulated by promoter region methylation. HOXD10 suppressed colony formation, cell proliferation, cell invasion and migration, and induced G2/M phase arrest and apoptosis in HCC cells. HOXD10 suppressed HCC cell xenograft growth in mice. HOXD10 suppresses HCC growth by inhibiting ERK signaling. Conclusion HOXD10 is frequently methylated in human HCC, and the expression of HOXD10 is regulated by promoter region methylation. HOXD10 suppresses HCC cell growth both in vitro and in vivo. HOXD10 suppresses human HCC by inhibiting ERK signaling. | ||
| 650 | 4 | |a HOXD10 | |
| 650 | 4 | |a DNA methylation | |
| 650 | 4 | |a Hepatocellular carcinoma | |
| 650 | 4 | |a IGFBP3 | |
| 650 | 4 | |a ERK1/2 | |
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| 700 | 0 | |a Weili Yang |e verfasserin |4 aut | |
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| 700 | 0 | |a Guanglong Dong |e verfasserin |4 aut | |
| 700 | 0 | |a Mingzhou Guo |e verfasserin |4 aut | |
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10.1186/s13148-017-0412-9 doi (DE-627)DOAJ077508769 (DE-599)DOAJ4a4c36fd6cc84d26bad5bebb3d35a2a9 DE-627 ger DE-627 rakwb eng QH426-470 Yulin Guo verfasserin aut Silencing HOXD10 by promoter region hypermethylation activates ERK signaling in hepatocellular carcinoma 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Hepatocellular carcinoma is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. Dysregulation of HomeoboxD10 (HOXD10) was found to suppress or promote cancer progression in different cancer types. The function and regulation of HOXD10 remain unclear in human hepatocellular carcinoma (HCC). Methods Primary HCC samples (117), normal liver tissue samples (15), and 13 HCC cell lines (SNU182, SNU449, HBXF344, SMMC7721, Huh7, HepG2, LM3, PLC/PRF/5, BEL7402, SNU387, SNU475, QGY7703, and Huh1) were included in this study. Methylation-specific PCR, flow cytometry, western blot, transwell, siRNA, and chromatin immunoprecipitation assays were employed. Results HOXD10 was methylated in 76.9% (90/117) of human primary HCC samples. HOXD10 methylation was significantly associated with vessel cancerous embolus, tumor cell differentiation, and the 3-year overall survival rate (all P < 0.05). The expression of HOXD10 was regulated by promoter region methylation. HOXD10 suppressed colony formation, cell proliferation, cell invasion and migration, and induced G2/M phase arrest and apoptosis in HCC cells. HOXD10 suppressed HCC cell xenograft growth in mice. HOXD10 suppresses HCC growth by inhibiting ERK signaling. Conclusion HOXD10 is frequently methylated in human HCC, and the expression of HOXD10 is regulated by promoter region methylation. HOXD10 suppresses HCC cell growth both in vitro and in vivo. HOXD10 suppresses human HCC by inhibiting ERK signaling. HOXD10 DNA methylation Hepatocellular carcinoma IGFBP3 ERK1/2 Medicine R Genetics Yaojun Peng verfasserin aut Dan Gao verfasserin aut Meiying Zhang verfasserin aut Weili Yang verfasserin aut Enqiang Linghu verfasserin aut James G. Herman verfasserin aut François Fuks verfasserin aut Guanglong Dong verfasserin aut Mingzhou Guo verfasserin aut In Clinical Epigenetics 9(2017), 1, Seite 13 volume:9 year:2017 number:1 pages:13 https://doi.org/10.1186/s13148-017-0412-9 kostenfrei https://doaj.org/article/4a4c36fd6cc84d26bad5bebb3d35a2a9 kostenfrei http://link.springer.com/article/10.1186/s13148-017-0412-9 kostenfrei https://doaj.org/toc/1868-7075 Journal toc kostenfrei https://doaj.org/toc/1868-7083 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 9 2017 1 13 |
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10.1186/s13148-017-0412-9 doi (DE-627)DOAJ077508769 (DE-599)DOAJ4a4c36fd6cc84d26bad5bebb3d35a2a9 DE-627 ger DE-627 rakwb eng QH426-470 Yulin Guo verfasserin aut Silencing HOXD10 by promoter region hypermethylation activates ERK signaling in hepatocellular carcinoma 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Hepatocellular carcinoma is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. Dysregulation of HomeoboxD10 (HOXD10) was found to suppress or promote cancer progression in different cancer types. The function and regulation of HOXD10 remain unclear in human hepatocellular carcinoma (HCC). Methods Primary HCC samples (117), normal liver tissue samples (15), and 13 HCC cell lines (SNU182, SNU449, HBXF344, SMMC7721, Huh7, HepG2, LM3, PLC/PRF/5, BEL7402, SNU387, SNU475, QGY7703, and Huh1) were included in this study. Methylation-specific PCR, flow cytometry, western blot, transwell, siRNA, and chromatin immunoprecipitation assays were employed. Results HOXD10 was methylated in 76.9% (90/117) of human primary HCC samples. HOXD10 methylation was significantly associated with vessel cancerous embolus, tumor cell differentiation, and the 3-year overall survival rate (all P < 0.05). The expression of HOXD10 was regulated by promoter region methylation. HOXD10 suppressed colony formation, cell proliferation, cell invasion and migration, and induced G2/M phase arrest and apoptosis in HCC cells. HOXD10 suppressed HCC cell xenograft growth in mice. HOXD10 suppresses HCC growth by inhibiting ERK signaling. Conclusion HOXD10 is frequently methylated in human HCC, and the expression of HOXD10 is regulated by promoter region methylation. HOXD10 suppresses HCC cell growth both in vitro and in vivo. HOXD10 suppresses human HCC by inhibiting ERK signaling. HOXD10 DNA methylation Hepatocellular carcinoma IGFBP3 ERK1/2 Medicine R Genetics Yaojun Peng verfasserin aut Dan Gao verfasserin aut Meiying Zhang verfasserin aut Weili Yang verfasserin aut Enqiang Linghu verfasserin aut James G. Herman verfasserin aut François Fuks verfasserin aut Guanglong Dong verfasserin aut Mingzhou Guo verfasserin aut In Clinical Epigenetics 9(2017), 1, Seite 13 volume:9 year:2017 number:1 pages:13 https://doi.org/10.1186/s13148-017-0412-9 kostenfrei https://doaj.org/article/4a4c36fd6cc84d26bad5bebb3d35a2a9 kostenfrei http://link.springer.com/article/10.1186/s13148-017-0412-9 kostenfrei https://doaj.org/toc/1868-7075 Journal toc kostenfrei https://doaj.org/toc/1868-7083 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 9 2017 1 13 |
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10.1186/s13148-017-0412-9 doi (DE-627)DOAJ077508769 (DE-599)DOAJ4a4c36fd6cc84d26bad5bebb3d35a2a9 DE-627 ger DE-627 rakwb eng QH426-470 Yulin Guo verfasserin aut Silencing HOXD10 by promoter region hypermethylation activates ERK signaling in hepatocellular carcinoma 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Hepatocellular carcinoma is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. Dysregulation of HomeoboxD10 (HOXD10) was found to suppress or promote cancer progression in different cancer types. The function and regulation of HOXD10 remain unclear in human hepatocellular carcinoma (HCC). Methods Primary HCC samples (117), normal liver tissue samples (15), and 13 HCC cell lines (SNU182, SNU449, HBXF344, SMMC7721, Huh7, HepG2, LM3, PLC/PRF/5, BEL7402, SNU387, SNU475, QGY7703, and Huh1) were included in this study. Methylation-specific PCR, flow cytometry, western blot, transwell, siRNA, and chromatin immunoprecipitation assays were employed. Results HOXD10 was methylated in 76.9% (90/117) of human primary HCC samples. HOXD10 methylation was significantly associated with vessel cancerous embolus, tumor cell differentiation, and the 3-year overall survival rate (all P < 0.05). The expression of HOXD10 was regulated by promoter region methylation. HOXD10 suppressed colony formation, cell proliferation, cell invasion and migration, and induced G2/M phase arrest and apoptosis in HCC cells. HOXD10 suppressed HCC cell xenograft growth in mice. HOXD10 suppresses HCC growth by inhibiting ERK signaling. Conclusion HOXD10 is frequently methylated in human HCC, and the expression of HOXD10 is regulated by promoter region methylation. HOXD10 suppresses HCC cell growth both in vitro and in vivo. HOXD10 suppresses human HCC by inhibiting ERK signaling. HOXD10 DNA methylation Hepatocellular carcinoma IGFBP3 ERK1/2 Medicine R Genetics Yaojun Peng verfasserin aut Dan Gao verfasserin aut Meiying Zhang verfasserin aut Weili Yang verfasserin aut Enqiang Linghu verfasserin aut James G. Herman verfasserin aut François Fuks verfasserin aut Guanglong Dong verfasserin aut Mingzhou Guo verfasserin aut In Clinical Epigenetics 9(2017), 1, Seite 13 volume:9 year:2017 number:1 pages:13 https://doi.org/10.1186/s13148-017-0412-9 kostenfrei https://doaj.org/article/4a4c36fd6cc84d26bad5bebb3d35a2a9 kostenfrei http://link.springer.com/article/10.1186/s13148-017-0412-9 kostenfrei https://doaj.org/toc/1868-7075 Journal toc kostenfrei https://doaj.org/toc/1868-7083 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 9 2017 1 13 |
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10.1186/s13148-017-0412-9 doi (DE-627)DOAJ077508769 (DE-599)DOAJ4a4c36fd6cc84d26bad5bebb3d35a2a9 DE-627 ger DE-627 rakwb eng QH426-470 Yulin Guo verfasserin aut Silencing HOXD10 by promoter region hypermethylation activates ERK signaling in hepatocellular carcinoma 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Hepatocellular carcinoma is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. Dysregulation of HomeoboxD10 (HOXD10) was found to suppress or promote cancer progression in different cancer types. The function and regulation of HOXD10 remain unclear in human hepatocellular carcinoma (HCC). Methods Primary HCC samples (117), normal liver tissue samples (15), and 13 HCC cell lines (SNU182, SNU449, HBXF344, SMMC7721, Huh7, HepG2, LM3, PLC/PRF/5, BEL7402, SNU387, SNU475, QGY7703, and Huh1) were included in this study. Methylation-specific PCR, flow cytometry, western blot, transwell, siRNA, and chromatin immunoprecipitation assays were employed. Results HOXD10 was methylated in 76.9% (90/117) of human primary HCC samples. HOXD10 methylation was significantly associated with vessel cancerous embolus, tumor cell differentiation, and the 3-year overall survival rate (all P < 0.05). The expression of HOXD10 was regulated by promoter region methylation. HOXD10 suppressed colony formation, cell proliferation, cell invasion and migration, and induced G2/M phase arrest and apoptosis in HCC cells. HOXD10 suppressed HCC cell xenograft growth in mice. HOXD10 suppresses HCC growth by inhibiting ERK signaling. Conclusion HOXD10 is frequently methylated in human HCC, and the expression of HOXD10 is regulated by promoter region methylation. HOXD10 suppresses HCC cell growth both in vitro and in vivo. HOXD10 suppresses human HCC by inhibiting ERK signaling. HOXD10 DNA methylation Hepatocellular carcinoma IGFBP3 ERK1/2 Medicine R Genetics Yaojun Peng verfasserin aut Dan Gao verfasserin aut Meiying Zhang verfasserin aut Weili Yang verfasserin aut Enqiang Linghu verfasserin aut James G. Herman verfasserin aut François Fuks verfasserin aut Guanglong Dong verfasserin aut Mingzhou Guo verfasserin aut In Clinical Epigenetics 9(2017), 1, Seite 13 volume:9 year:2017 number:1 pages:13 https://doi.org/10.1186/s13148-017-0412-9 kostenfrei https://doaj.org/article/4a4c36fd6cc84d26bad5bebb3d35a2a9 kostenfrei http://link.springer.com/article/10.1186/s13148-017-0412-9 kostenfrei https://doaj.org/toc/1868-7075 Journal toc kostenfrei https://doaj.org/toc/1868-7083 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 9 2017 1 13 |
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10.1186/s13148-017-0412-9 doi (DE-627)DOAJ077508769 (DE-599)DOAJ4a4c36fd6cc84d26bad5bebb3d35a2a9 DE-627 ger DE-627 rakwb eng QH426-470 Yulin Guo verfasserin aut Silencing HOXD10 by promoter region hypermethylation activates ERK signaling in hepatocellular carcinoma 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Hepatocellular carcinoma is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. Dysregulation of HomeoboxD10 (HOXD10) was found to suppress or promote cancer progression in different cancer types. The function and regulation of HOXD10 remain unclear in human hepatocellular carcinoma (HCC). Methods Primary HCC samples (117), normal liver tissue samples (15), and 13 HCC cell lines (SNU182, SNU449, HBXF344, SMMC7721, Huh7, HepG2, LM3, PLC/PRF/5, BEL7402, SNU387, SNU475, QGY7703, and Huh1) were included in this study. Methylation-specific PCR, flow cytometry, western blot, transwell, siRNA, and chromatin immunoprecipitation assays were employed. Results HOXD10 was methylated in 76.9% (90/117) of human primary HCC samples. HOXD10 methylation was significantly associated with vessel cancerous embolus, tumor cell differentiation, and the 3-year overall survival rate (all P < 0.05). The expression of HOXD10 was regulated by promoter region methylation. HOXD10 suppressed colony formation, cell proliferation, cell invasion and migration, and induced G2/M phase arrest and apoptosis in HCC cells. HOXD10 suppressed HCC cell xenograft growth in mice. HOXD10 suppresses HCC growth by inhibiting ERK signaling. Conclusion HOXD10 is frequently methylated in human HCC, and the expression of HOXD10 is regulated by promoter region methylation. HOXD10 suppresses HCC cell growth both in vitro and in vivo. HOXD10 suppresses human HCC by inhibiting ERK signaling. HOXD10 DNA methylation Hepatocellular carcinoma IGFBP3 ERK1/2 Medicine R Genetics Yaojun Peng verfasserin aut Dan Gao verfasserin aut Meiying Zhang verfasserin aut Weili Yang verfasserin aut Enqiang Linghu verfasserin aut James G. Herman verfasserin aut François Fuks verfasserin aut Guanglong Dong verfasserin aut Mingzhou Guo verfasserin aut In Clinical Epigenetics 9(2017), 1, Seite 13 volume:9 year:2017 number:1 pages:13 https://doi.org/10.1186/s13148-017-0412-9 kostenfrei https://doaj.org/article/4a4c36fd6cc84d26bad5bebb3d35a2a9 kostenfrei http://link.springer.com/article/10.1186/s13148-017-0412-9 kostenfrei https://doaj.org/toc/1868-7075 Journal toc kostenfrei https://doaj.org/toc/1868-7083 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 9 2017 1 13 |
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Dysregulation of HomeoboxD10 (HOXD10) was found to suppress or promote cancer progression in different cancer types. The function and regulation of HOXD10 remain unclear in human hepatocellular carcinoma (HCC). Methods Primary HCC samples (117), normal liver tissue samples (15), and 13 HCC cell lines (SNU182, SNU449, HBXF344, SMMC7721, Huh7, HepG2, LM3, PLC/PRF/5, BEL7402, SNU387, SNU475, QGY7703, and Huh1) were included in this study. Methylation-specific PCR, flow cytometry, western blot, transwell, siRNA, and chromatin immunoprecipitation assays were employed. Results HOXD10 was methylated in 76.9% (90/117) of human primary HCC samples. HOXD10 methylation was significantly associated with vessel cancerous embolus, tumor cell differentiation, and the 3-year overall survival rate (all P < 0.05). The expression of HOXD10 was regulated by promoter region methylation. 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Silencing HOXD10 by promoter region hypermethylation activates ERK signaling in hepatocellular carcinoma |
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Yulin Guo Yaojun Peng Dan Gao Meiying Zhang Weili Yang Enqiang Linghu James G. Herman François Fuks Guanglong Dong Mingzhou Guo |
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silencing hoxd10 by promoter region hypermethylation activates erk signaling in hepatocellular carcinoma |
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QH426-470 |
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Silencing HOXD10 by promoter region hypermethylation activates ERK signaling in hepatocellular carcinoma |
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Abstract Background Hepatocellular carcinoma is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. Dysregulation of HomeoboxD10 (HOXD10) was found to suppress or promote cancer progression in different cancer types. The function and regulation of HOXD10 remain unclear in human hepatocellular carcinoma (HCC). Methods Primary HCC samples (117), normal liver tissue samples (15), and 13 HCC cell lines (SNU182, SNU449, HBXF344, SMMC7721, Huh7, HepG2, LM3, PLC/PRF/5, BEL7402, SNU387, SNU475, QGY7703, and Huh1) were included in this study. Methylation-specific PCR, flow cytometry, western blot, transwell, siRNA, and chromatin immunoprecipitation assays were employed. Results HOXD10 was methylated in 76.9% (90/117) of human primary HCC samples. HOXD10 methylation was significantly associated with vessel cancerous embolus, tumor cell differentiation, and the 3-year overall survival rate (all P < 0.05). The expression of HOXD10 was regulated by promoter region methylation. HOXD10 suppressed colony formation, cell proliferation, cell invasion and migration, and induced G2/M phase arrest and apoptosis in HCC cells. HOXD10 suppressed HCC cell xenograft growth in mice. HOXD10 suppresses HCC growth by inhibiting ERK signaling. Conclusion HOXD10 is frequently methylated in human HCC, and the expression of HOXD10 is regulated by promoter region methylation. HOXD10 suppresses HCC cell growth both in vitro and in vivo. HOXD10 suppresses human HCC by inhibiting ERK signaling. |
| abstractGer |
Abstract Background Hepatocellular carcinoma is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. Dysregulation of HomeoboxD10 (HOXD10) was found to suppress or promote cancer progression in different cancer types. The function and regulation of HOXD10 remain unclear in human hepatocellular carcinoma (HCC). Methods Primary HCC samples (117), normal liver tissue samples (15), and 13 HCC cell lines (SNU182, SNU449, HBXF344, SMMC7721, Huh7, HepG2, LM3, PLC/PRF/5, BEL7402, SNU387, SNU475, QGY7703, and Huh1) were included in this study. Methylation-specific PCR, flow cytometry, western blot, transwell, siRNA, and chromatin immunoprecipitation assays were employed. Results HOXD10 was methylated in 76.9% (90/117) of human primary HCC samples. HOXD10 methylation was significantly associated with vessel cancerous embolus, tumor cell differentiation, and the 3-year overall survival rate (all P < 0.05). The expression of HOXD10 was regulated by promoter region methylation. HOXD10 suppressed colony formation, cell proliferation, cell invasion and migration, and induced G2/M phase arrest and apoptosis in HCC cells. HOXD10 suppressed HCC cell xenograft growth in mice. HOXD10 suppresses HCC growth by inhibiting ERK signaling. Conclusion HOXD10 is frequently methylated in human HCC, and the expression of HOXD10 is regulated by promoter region methylation. HOXD10 suppresses HCC cell growth both in vitro and in vivo. HOXD10 suppresses human HCC by inhibiting ERK signaling. |
| abstract_unstemmed |
Abstract Background Hepatocellular carcinoma is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. Dysregulation of HomeoboxD10 (HOXD10) was found to suppress or promote cancer progression in different cancer types. The function and regulation of HOXD10 remain unclear in human hepatocellular carcinoma (HCC). Methods Primary HCC samples (117), normal liver tissue samples (15), and 13 HCC cell lines (SNU182, SNU449, HBXF344, SMMC7721, Huh7, HepG2, LM3, PLC/PRF/5, BEL7402, SNU387, SNU475, QGY7703, and Huh1) were included in this study. Methylation-specific PCR, flow cytometry, western blot, transwell, siRNA, and chromatin immunoprecipitation assays were employed. Results HOXD10 was methylated in 76.9% (90/117) of human primary HCC samples. HOXD10 methylation was significantly associated with vessel cancerous embolus, tumor cell differentiation, and the 3-year overall survival rate (all P < 0.05). The expression of HOXD10 was regulated by promoter region methylation. HOXD10 suppressed colony formation, cell proliferation, cell invasion and migration, and induced G2/M phase arrest and apoptosis in HCC cells. HOXD10 suppressed HCC cell xenograft growth in mice. HOXD10 suppresses HCC growth by inhibiting ERK signaling. Conclusion HOXD10 is frequently methylated in human HCC, and the expression of HOXD10 is regulated by promoter region methylation. HOXD10 suppresses HCC cell growth both in vitro and in vivo. HOXD10 suppresses human HCC by inhibiting ERK signaling. |
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Yaojun Peng Dan Gao Meiying Zhang Weili Yang Enqiang Linghu James G. Herman François Fuks Guanglong Dong Mingzhou Guo |
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