Deleted in liver cancer 2 (DLC2) was dispensable for development and its deficiency did not aggravate hepatocarcinogenesis
| Autor: | Amy K. M. Lam, Irene Oi-Lin Ng, Sandra Lam, Sookja K. Chung, Edmund Kwok-Kwan Tung, Tai-On Yau, Oi Fung Cheung, Thomas Ho-Yin Leung, Pek-Lan Khong |
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| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
Liver tumor
Tumor Suppressor Proteins - genetics - physiology Adipose tissue Fluorescent Antibody Technique lcsh:Medicine Oncology/Gastrointestinal Cancers Biology law.invention Mice Liver Neoplasms Experimental law Pregnancy medicine Animals Adipose Tissue - physiology Diethylnitrosamine lcsh:Science Molecular Biology Cells Cultured DNA Primers Mice Knockout Multidisciplinary Base Sequence Tumor Suppressor Proteins lcsh:R Liver Neoplasms Experimental - chemically induced - physiopathology Cell Biology medicine.disease Molecular biology Phenotype Adipose Tissue Adipogenesis Hepatocellular carcinoma Cancer research Suppressor Female lcsh:Q DLC1 Liver cancer Research Article |
| Zdroj: | PLoS ONE, Vol 4, Iss 8, p e6566 (2009) PLoS ONE |
| Popis: | DLC2 (deleted in liver cancer 2), a Rho GTPase-activating protein, was previously shown to be underexpressed in human hepatocellular carcinoma and has tumor suppressor functions in cell culture models. We generated DLC2-deficient mice to investigate the tumor suppressor role of DLC2 in hepatocarcinogenesis and the function of DLC2 in vivo. In this study, we found that, unlike homologous DLC1, which is essential for embryonic development, DLC2 was dispensable for embryonic development and DLC2-deficient mice could survive to adulthood. We also did not observe a higher incidence of liver tumor formation or diethylnitrosamine (DEN)-induced hepatocarcinogenesis in DLC2-deficient mice. However, we observed that DLC2-deficient mice were smaller and had less adipose tissue than the wild type mice. These phenotypes were not due to reduction of cell size or defect in adipogenesis, as observed in the 190B RhoGAP-deficient mouse model. Together, these results suggest that deficiency in DLC2 alone does not enhance hepatocarcinogenesis. © 2009 Yau et al. published_or_final_version |
| Databáze: | OpenAIRE |
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