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An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
Published on: September 12, 2019
Mitogen-activated protein kinases in hepatocellular carcinoma development
Lihua Min1, Baokun He, Lijian Hui
1Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy for Sciences, Yueyang Road 320, 200031 Shanghai, China.
Seminars in Cancer Biology
|October 26, 2010
Summary
Mitogen-activated protein kinases (MAPKs) like ERK, JNK, and p38 are crucial in liver cancer. Understanding these pathways offers new therapeutic targets for hepatocellular carcinoma (HCC) treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cell Signaling
Background:
- Hepatocellular carcinoma (HCC) is a major global cancer burden.
- Signaling pathways are key to understanding liver carcinogenesis and developing therapies.
- Mitogen-activated protein kinases (MAPKs) regulate essential cellular functions.
Purpose of the Study:
- To review recent findings on ERK, JNK, and p38 MAPK pathways in HCC development.
- To explore the therapeutic potential of targeting these MAPK pathways in HCC.
Main Methods:
- Literature review of studies on MAPK signaling in HCC.
- Analysis of mouse models investigating JNK and p38 functions in HCC.
- Discussion of the role of ERK pathway in HCC targeted therapy.
Main Results:
- Deregulated MAPKs contribute to HCC development.
- The ERK pathway has led to targeted therapies like Sorafenib.
- JNK and p38 pathways are increasingly recognized for their roles in HCC.
Conclusions:
- MAPK signaling pathways (ERK, JNK, p38) are critical in hepatocellular carcinoma.
- These pathways represent promising therapeutic targets for novel HCC treatments.
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