Mechanisms of Liver Carcinogenesis by Antiestrogens

2009 ◽  
pp. 69-81
Author(s):  
David H. Phillips
Keyword(s):  
Liver Carcinogenesis

RAGE is required for oval cell activation and inflammation-associated mouse liver carcinogenesis

2012 ◽  
Vol 50 (01) ◽  
Author(s):  
T Pusterla ◽  
J Németh ◽  
I Stein ◽  
L Wiechert ◽  
D Knigin ◽  
...  
Keyword(s):  
Mouse Liver ◽  
Cell Activation ◽  
Oval Cell ◽  
Liver Carcinogenesis

Overexpression of SMAD7 activates the YAP/NOTCH cascade and promotes liver carcinogenesis in mice and humans

Hepatology ◽  
2020 ◽  
Author(s):  
Haichuan Wang ◽  
Xinhua Song ◽  
Haotian Liao ◽  
Pan Wang ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Liver Carcinogenesis

scholarly journals Knockout of Putative Tumor Suppressor Aldh1l1 in Mice Reprograms Metabolism to Accelerate Growth of Tumors in a Diethylnitrosamine (DEN) Model of Liver Carcinogenesis

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3219
Author(s):  
Natalia I. Krupenko ◽  
Jaspreet Sharma ◽  
Halle M. Fogle ◽  
Peter Pediaditakis ◽  
Kyle C. Strickland ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Chemical Carcinogenesis ◽  
Dependent Manner ◽  
Wild Type ◽  
Liver Carcinogenesis ◽  
Wild Type Littermate ◽  
Tumor Multiplicity ◽  
Accelerate Growth ◽  
Putative Tumor Suppressor ◽  
Formyltetrahydrofolate Dehydrogenase

Cytosolic 10-formyltetrahydrofolate dehydrogenase (ALDH1L1) is commonly downregulated in human cancers through promoter methylation. We proposed that ALDH1L1 loss promotes malignant tumor growth. Here, we investigated the effect of the Aldh1l1 mouse knockout (Aldh1l1−/−) on hepatocellular carcinoma using a chemical carcinogenesis model. Fifteen-day-old male Aldh1l1 knockout mice and their wild-type littermate controls (Aldh1l1+/+) were injected intraperitoneally with 20 μg/g body weight of DEN (diethylnitrosamine). Mice were sacrificed 10, 20, 28, and 36 weeks post-DEN injection, and livers were examined for tumor multiplicity and size. We observed that while tumor multiplicity did not differ between Aldh1l1−/− and Aldh1l1+/+ animals, larger tumors grew in Aldh1l1−/− compared to Aldh1l1+/+ mice at 28 and 36 weeks. Profound differences between Aldh1l1−/− and Aldh1l1+/+ mice in the expression of inflammation-related genes were seen at 10 and 20 weeks. Of note, large tumors from wild-type mice showed a strong decrease of ALDH1L1 protein at 36 weeks. Metabolomic analysis of liver tissues at 20 weeks showed stronger differences in Aldh1l1+/+ versus Aldh1l1−/− metabotypes than at 10 weeks, which underscores metabolic pathways that respond to DEN in an ALDH1L1-dependent manner. Our study indicates that Aldh1l1 knockout promoted liver tumor growth without affecting tumor initiation or multiplicity.

scholarly journals Enrichment of progenitor cells by 2‐acetylaminofluorene accelerates liver carcinogenesis induced by diethylnitrosamine in vivo

2021 ◽  
Author(s):  
María Paulette Castro‐Gil ◽  
Ricardo Sánchez‐Rodríguez ◽  
Julia Esperanza Torres‐Mena ◽  
Carlos David López‐Torres ◽  
Valeria Quintanar‐Jurado ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Liver Carcinogenesis

scholarly journals A positive-feedback loop between HBx and ALKBH5 promotes hepatocellular carcinogenesis

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Siming Qu ◽  
Li Jin ◽  
Hanfei Huang ◽  
Jie Lin ◽  
Weiwu Gao ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
Hbv Infection ◽  
Cell Counting ◽  
Regulation Mechanism ◽  
Dependent Manner ◽  
Liver Carcinogenesis ◽  
Nude Mouse Model ◽  
Positive Feedback Loop

Abstract Background Hepatitis B Virus (HBV) contributes to liver carcinogenesis via various epigenetic mechanisms. The newly defined epigenetics, epitranscriptomics regulation, has been reported to involve in multiple cancers including Hepatocellular Carcinoma (HCC). Our previous study found that HBx, HBV encodes X protein, mediated H3K4me3 modification in WDR5-dependent manner to involve in HBV infection and contribute to oncogene expression. AlkB Homolog 5 (ALKBH5), one of epitranscriptomics enzymes, has been identified to be associated with various cancers. However, whether and how ALKBH5 is dysregulated in HBV-related HCC remains unclear yet. This study aims to investigate ALKBH5 function, clinical significance and mechanism in HBV related HCC (HBV-HCC) patients derived from Chinese people. Methods The expression pattern of ALKBH5 was evaluated by RT-qPCR, Western blot, data mining and immunohistochemistry in total of 373 HBV-HCC tissues and four HCC cell lines. Cell Counting Kit 8 (CCK8) assay, Transwell and nude mouse model were performed to assess ALKBH5 function by both small interference RNAs and lentiviral particles. The regulation mechanism of ALKBH5 was determined in HBx and WDR5 knockdown cells by CHIP-qPCR. The role of ALKBH5 in HBx mRNA N6-methyladenosine (m6A) modification was further evaluated by MeRIP-qPCR and Actinomycin D inhibitor experiment in HBV-driven cells and HBx overexpression cells. Result ALKBH5 increased in tumor tissues and predicts a poor prognosis of HBV-HCC. Mechanically, the highly expressed ALKBH5 is induced by HBx-mediated H3K4me3 modification of ALKBH5 gene promoter in a WDR5-dependent manner after HBV infection. The increased ALKBH5 protein catalyzes the m6A demethylation of HBx mRNA, thus stabilizing and favoring a higher HBx expression level. Furthermore, there are positive correlations between HBx and ALKBH5 in HBV-HCC tissues, and depletion of ALKBH5 significantly inhibits HBV-driven tumor cells’ growth and migration in vitro and in vivo. Conclusions HBx-ALKBH5 may form a positive-feedback loop to involve in the HBV-induced liver carcinogenesis, and targeting the loop at ALKBH5 may provide a potential way for HBV-HCC treatment.

Hypomethylation of LIMD1 and P16 by downregulation of DNMT1 results in restriction of liver carcinogenesis by amarogentin treatment

2021 ◽  
Vol 46 (3) ◽  
Author(s):  
Debolina Pal ◽  
Subhayan Sur ◽  
Rituparna Roy ◽  
Suvra Mandal ◽  
Chinmay Kumar Panda
Keyword(s):  
Liver Carcinogenesis

Lack of modifying effects of 6-mercaptopurine in a medium term bioassay system for liver carcinogenesis using male F344 rats

1992 ◽  
Vol 64 (2) ◽  
pp. 99-107
Author(s):  
Toshihiro Amanuma ◽  
Hiroshi Maruyama ◽  
Toshifumi Tsujiuchi ◽  
Masahiro Tsutsumi ◽  
Ayumi Denda ◽  
...  
Keyword(s):  
Liver Carcinogenesis ◽  
Medium Term ◽  
Bioassay System ◽  
F344 Rats ◽  
Male F344 Rats

Effects of griseofulvin in medium-term liver carcinogenesis assay and peripheral blood micronucleus test in rat

2001 ◽  
Vol 21 (6) ◽  
pp. 441-451 ◽  
Author(s):  
Karine Labay ◽  
Mostafa Ould-Elhkim ◽  
Virginie Klés ◽  
Magali Guffroy ◽  
Jean-Michel Poul ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Micronucleus Test ◽  
Liver Carcinogenesis ◽  
Medium Term
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