Effect of DEN-induced liver cancer in wildtype and OTUD3 knockout mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE266622 | GEO | 2024/07/10
REPOSITORIES: GEO
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Project description:Liver carcinogenesis induced by DEN closely mimics the pathologies observed during human liver tumor initiation and progression. DEN treatment triggered c-Jun expression lasting up to at least 1 week in mouse livers as measured by Western blots and immunohistochemical staining. DEN-induced liver tumorigenesis was also dramatically reduced in Alfp-cre+/c-jun f/f mice, in which c-Jun is constitutively deleted in hepatocytes around birth. These data unambiguously demonstrate that c-Jun is specifically required during liver cancer initiation. We searched for cell death effectors downstream of c-Jun operating in cancer initiation. Expression profiling revealed that several cell death-associated genes were deregulated by comparing Alfp-cre+/c-junf/f and Alfp-cre-/c-jun f/f livers. Mouse livers were collected before and 48hours after diethylnitrosamine treament (100mg/kg body weight). Whole genome expression profiles were analyzed using total RNAs extracted from the whole liver samples.
2012-08-08 | GSE39931 | GEO
Project description:Liver carcinogenesis induced by DEN closely mimics the pathologies observed during human liver tumor initiation and progression. DEN treatment triggered c-Jun expression lasting up to at least 1 week in mouse livers as measured by Western blots and immunohistochemical staining. DEN-induced liver tumorigenesis was also dramatically reduced in Alfp-cre+/c-jun f/f mice, in which c-Jun is constitutively deleted in hepatocytes around birth. These data unambiguously demonstrate that c-Jun is specifically required during liver cancer initiation. We searched for cell death effectors downstream of c-Jun operating in cancer initiation. Expression profiling revealed that several cell death-associated genes were deregulated by comparing Alfp-cre+/c-junf/f and Alfp-cre-/c-jun f/f livers. Mouse livers were collected before and 48hours after diethylnitrosamine treament (100mg/kg body weight). Whole genome expression profiles were analyzed using total RNAs extracted from the whole liver samples.
2012-08-08 | GSE39930 | GEO
Project description:Liver carcinogenesis induced by DEN closely mimics the pathologies observed during human liver tumor initiation and progression. DEN treatment triggered c-Jun expression lasting up to at least 1 week in mouse livers as measured by Western blots and immunohistochemical staining. DEN-induced liver tumorigenesis was also dramatically reduced in Alfp-cre+/c-jun f/f mice, in which c-Jun is constitutively deleted in hepatocytes around birth. These data unambiguously demonstrate that c-Jun is specifically required during liver cancer initiation. We searched for cell death effectors downstream of c-Jun operating in cancer initiation. Expression profiling revealed that several cell death-associated genes were deregulated by comparing Alfp-cre+/c-junf/f and Alfp-cre-/c-jun f/f livers. Mouse livers were collected before and 48hours after diethylnitrosamine treament (100mg/kg body weight). Whole genome expression profiles were analyzed using total RNAs extracted from the whole liver samples.
2012-08-08 | GSE39929 | GEO
Project description:Liver carcinogenesis induced by DEN closely mimics the pathologies observed during human liver tumor initiation and progression. DEN treatment triggered c-Jun expression lasting up to at least 1 week in mouse livers as measured by Western blots and immunohistochemical staining. DEN-induced liver tumorigenesis was also dramatically reduced in Alfp-cre+/c-jun f/f mice, in which c-Jun is constitutively deleted in hepatocytes around birth. These data unambiguously demonstrate that c-Jun is specifically required during liver cancer initiation. We searched for cell death effectors downstream of c-Jun operating in cancer initiation. Expression profiling revealed that several cell death-associated genes were deregulated by comparing Alfp-cre+/c-junf/f and Alfp-cre-/c-jun f/f livers. Mouse livers were collected before and 48hours after diethylnitrosamine treament (100mg/kg body weight). Whole genome expression profiles were analyzed using total RNAs extracted from the whole liver samples.
2012-08-08 | GSE39928 | GEO
Project description:Single nucleotide polymorphisms in the FTO gene encoding a m6A demthylase are associated with obesity and cancer development. However, the functional role of FTO in the developemnt of progression of hepatocellular carcinoma (HCC) as a proteotypic obesity-associated cancer remains unclear. Here, we have generated mice with hepatic FTO deficiency (FTOL-KO) and subjected them to DEN induced HCC-development. FTOL-KO mice exhibit increased HCC burden. While control mice exhibit a dynamic regulation of FTO upon induction of liver damage, this response is abrogated in mice lacking FTO. Proteomic analyses revealed that liver damage-induced increases in FTO expression promotes m6A-demethylation of CUL4A reducing its protein expression. Functionally, knockdown of CUL4A restores the increased hepatocyte proliferation observed upon loss of FTO. Collectively, our study reveals a protective role for FTO-dependent dynamic m6A mRNA demethylation of CUL4A in the initiation of HCC development.
2020-11-03 | PXD018223 | Pride
Project description:Liver carcinogenesis induced by DEN closely mimics the pathologies observed during human liver tumor initiation and progression. DEN treatment triggered c-Jun expression lasting up to at least 1 week in mouse livers as measured by Western blots and immunohistochemical staining. DEN-induced liver tumorigenesis was also dramatically reduced in Alfp-cre+/c-jun f/f mice, in which c-Jun is constitutively deleted in hepatocytes around birth. These data unambiguously demonstrate that c-Jun is specifically required during liver cancer initiation. We searched for cell death effectors downstream of c-Jun operating in cancer initiation. Expression profiling revealed that several cell death-associated genes were deregulated by comparing Alfp-cre+/c-junf/f and Alfp-cre-/c-jun f/f livers. Mouse livers were collected before and 48hours after diethylnitrosamine treament (100mg/kg body weight). Whole genome expression profiles were analyzed using total RNAs extracted from the whole liver samples. By comparison of the gene expression profiles of these samples, genes with significantly altered expression levels will be selected and further characterized for their roles in DEN-induce liver cell death in tumor initiation.
2012-08-07 | E-GEOD-39930 | biostudies-arrayexpress
Project description:Liver carcinogenesis induced by DEN closely mimics the pathologies observed during human liver tumor initiation and progression. DEN treatment triggered c-Jun expression lasting up to at least 1 week in mouse livers as measured by Western blots and immunohistochemical staining. DEN-induced liver tumorigenesis was also dramatically reduced in Alfp-cre+/c-jun f/f mice, in which c-Jun is constitutively deleted in hepatocytes around birth. These data unambiguously demonstrate that c-Jun is specifically required during liver cancer initiation. We searched for cell death effectors downstream of c-Jun operating in cancer initiation. Expression profiling revealed that several cell death-associated genes were deregulated by comparing Alfp-cre+/c-junf/f and Alfp-cre-/c-jun f/f livers. Mouse livers were collected before and 48hours after diethylnitrosamine treament (100mg/kg body weight). Whole genome expression profiles were analyzed using total RNAs extracted from the whole liver samples. By comparison of the gene expression profiles of these samples, genes with significantly altered expression levels will be selected and further characterized for their roles in DEN-induce liver cell death in tumor initiation.
2012-08-07 | E-GEOD-39929 | biostudies-arrayexpress
Project description:Liver carcinogenesis induced by DEN closely mimics the pathologies observed during human liver tumor initiation and progression. DEN treatment triggered c-Jun expression lasting up to at least 1 week in mouse livers as measured by Western blots and immunohistochemical staining. DEN-induced liver tumorigenesis was also dramatically reduced in Alfp-cre+/c-jun f/f mice, in which c-Jun is constitutively deleted in hepatocytes around birth. These data unambiguously demonstrate that c-Jun is specifically required during liver cancer initiation. We searched for cell death effectors downstream of c-Jun operating in cancer initiation. Expression profiling revealed that several cell death-associated genes were deregulated by comparing Alfp-cre+/c-junf/f and Alfp-cre-/c-jun f/f livers. Mouse livers were collected before and 48hours after diethylnitrosamine treament (100mg/kg body weight). Whole genome expression profiles were analyzed using total RNAs extracted from the whole liver samples. By comparison of the gene expression profiles of these samples, genes with significantly altered expression levels will be selected and further characterized for their roles in DEN-induce liver cell death in tumor initiation.
2012-08-07 | E-GEOD-39931 | biostudies-arrayexpress
Project description:Liver carcinogenesis induced by DEN closely mimics the pathologies observed during human liver tumor initiation and progression. DEN treatment triggered c-Jun expression lasting up to at least 1 week in mouse livers as measured by Western blots and immunohistochemical staining. DEN-induced liver tumorigenesis was also dramatically reduced in Alfp-cre+/c-jun f/f mice, in which c-Jun is constitutively deleted in hepatocytes around birth. These data unambiguously demonstrate that c-Jun is specifically required during liver cancer initiation. We searched for cell death effectors downstream of c-Jun operating in cancer initiation. Expression profiling revealed that several cell death-associated genes were deregulated by comparing Alfp-cre+/c-junf/f and Alfp-cre-/c-jun f/f livers. Mouse livers were collected before and 48hours after diethylnitrosamine treament (100mg/kg body weight). Whole genome expression profiles were analyzed using total RNAs extracted from the whole liver samples. By comparison of the gene expression profiles of these samples, genes with significantly altered expression levels will be selected and further characterized for their roles in DEN-induce liver cell death in tumor initiation.
2012-08-07 | E-GEOD-39928 | biostudies-arrayexpress
Project description:Hepatocellular carcinoma is the third leading cause of cancer death worldwide, and it is necessary to elucidate the mechanism of hepatocarcinogenesis. Hepatocellular carcinoma (HCC) has a high mortality rate and develops based on the chronic inflammatory hepatic disease. Therefore, novel prophylactic or therapeutic strategies are required to improve outcome. In this study, influence of diethylnitrosamine (DEN) and retinoic acid (ATRA) on hepatocarcinogenesis was investigated in mouse. These results suggest that the control of NF-M-NM-:B signaling during the early stage of HCC development is important for the prevention of malignant transformation in hepatocytes. Genes induced by the following treatments in mice liver were investigated at 2 days or 7 days after treatment; DEN: diethylnitrosamine (treatment of DEN (drinking water 80 mg/L)) ATRA: retinoic acid (treatment of ATRA (drinking water 30 mg/L)) G0s2 siRNA : G0s2 knockdown mouse liver (treatment of G0s2 siRNA) Control siRNA: treatment of scramble siRNA (negative control)
2014-06-06 | E-GEOD-57798 | biostudies-arrayexpress