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Delta-like ligand 4 in hepatocellular carcinoma intrinsically promotes tumour growth and suppresses hepatitis B virus replication.
Kunanopparat, Areerat; Issara-Amphorn, Jiraphorn; Leelahavanichkul, Asada; Sanpavat, Anapat; Patumraj, Suthiluk; Tangkijvanich, Pisit; Palaga, Tanapat; Hirankarn, Nattiya.
Afiliación
  • Kunanopparat A; Center of Excellence in Immunology and Immune Mediated Diseases, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
  • Issara-Amphorn J; Center of Excellence in Immunology and Immune Mediated Diseases, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
  • Leelahavanichkul A; Center of Excellence in Immunology and Immune Mediated Diseases, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
  • Sanpavat A; Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
  • Patumraj S; Center of Excellence for Microcirculation, Department of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
  • Tangkijvanich P; Research Unit of Hepatitis and Liver Cancer, Department of Biochemistry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
  • Palaga T; Department of Microbiology, Faculty of Science, Chulalongkorn University, Bangkok 10330, Thailand.
  • Hirankarn N; Center of Excellence in Immunology and Immune Mediated Diseases, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand. nattiya.H@chula.ac.th.
World J Gastroenterol ; 24(34): 3861-3870, 2018 Sep 14.
Article en En | MEDLINE | ID: mdl-30228780
AIM: To investigate the role of Delta-like ligand 4 (DLL4) on tumour growth in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC) in vivo. METHODS: We suppressed DLL4 expression in an HBV expressing HCC cell line, HepG2.2.15 and analysed the growth ability of cells as subcutaneous tumours in nude mice. The expression of tumour angiogenesis regulators, VEGF-A and VEGF-R2 in tumour xenografts were examined by western blotting. The tumour proliferation and neovasculature were examined by immunohistochemistry. The viral replication and viral protein expression were measured by quantitative PCR and western blotting, respectively. RESULTS: Eighteen days after implantation, tumour volume in mice implanted with shDLL4 HepG2.2.15 was significantly smaller than in mice implanted with control HepG2.2.15 (P < 0.0001). The levels of angiogenesis regulators, VEGF-A and VEGF-R2 were significantly decreased in implanted tumours with suppressed DLL4 compared with the control group (P < 0.001 and P < 0.05, respectively). Furthermore, the suppression of DLL4 expression in tumour cells reduced cell proliferation and the formation of new blood vessels in tumours. Unexpectedly, increased viral replication was observed after suppression of DLL4 in the tumours. CONCLUSION: This study demonstrates that DLL4 is important in regulating the tumour growth of HBV-associated HCC as well as the neovascularization and suppression of HBV replication.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Replicación Viral / Virus de la Hepatitis B / Carcinoma Hepatocelular / Péptidos y Proteínas de Señalización Intercelular / Neoplasias Hepáticas Tipo de estudio: Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: World J Gastroenterol Asunto de la revista: GASTROENTEROLOGIA Año: 2018 Tipo del documento: Article País de afiliación: Tailandia Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Replicación Viral / Virus de la Hepatitis B / Carcinoma Hepatocelular / Péptidos y Proteínas de Señalización Intercelular / Neoplasias Hepáticas Tipo de estudio: Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: World J Gastroenterol Asunto de la revista: GASTROENTEROLOGIA Año: 2018 Tipo del documento: Article País de afiliación: Tailandia Pais de publicación: Estados Unidos