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A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
Published on: July 6, 2017
Transgenic CHD1L expression in mouse induces spontaneous tumors
Muhan Chen1, Jian-dong Huang, Liang Hu
1Department of Clinical Oncology, The University of Hong Kong, Pokfulam, Hong Kong, China.
Plos One
|August 25, 2009
Summary
Chromosome 1q21 amplification drives hepatocellular carcinoma (HCC). The CHD1L oncogene promotes HCC tumor growth and proliferation by regulating cell cycle progression, supporting its role in liver cancer pathogenesis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Hepatocellular carcinoma (HCC) frequently exhibits 1q21 amplification, a common genetic alteration.
- The candidate oncogene CHD1L, isolated from the 1q21 region, demonstrates significant oncogenic potential.
- Previous research indicated CHD1L promotes cell proliferation, a key factor in tumorigenesis.
Purpose of the Study:
- To investigate the in vivo oncogenic role of CHD1L in hepatocellular carcinoma.
- To explore the mechanism by which CHD1L promotes cell proliferation and tumor development.
Main Methods:
- Generation of a CHD1L ubiquitous-expression transgenic mouse model.
- Induction of hepatocyte lesions using alcohol intoxication in transgenic and wild-type mice.
- Flow cytometry analysis of mouse embryo fibroblasts (MEFs) to assess cell cycle progression.
Main Results:
- Spontaneous tumor formation, including HCC, observed in 24.4% of CHD1L-transgenic mice.
- Overexpression of CHD1L enhanced susceptibility to alcohol-induced liver lesions and tumor development.
- CHD1L facilitated DNA synthesis and G1/S transition by modulating key cell cycle regulators (Cyclins, CDKs, Rb, p27Kip1, p53).
Conclusions:
- CHD1L is confirmed as a novel oncogene.
- CHD1L plays a critical role in the pathogenesis of hepatocellular carcinoma.
