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Updated: Apr 17, 2026
10:37
Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
36.8K
MAPK7 Regulates EMT Features and Modulates the Generation of CTCs
Sarah Javaid1, Jianmin Zhang2, Gromoslaw A Smolen2
1Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts. Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts.
Molecular Cancer Research : MCR
|February 14, 2015
Summary
Targeting mitogen-activated protein kinase 7 (MAPK7) can reverse tumor cell invasion. Suppressing MAPK7 promotes epithelial markers and reduces metastasis, offering a potential therapeutic strategy for cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Epithelial-to-mesenchymal transition (EMT) is crucial for tumor cell migration, invasion, and metastasis.
- Identifying therapeutic targets to reverse EMT is a key challenge in cancer research.
Purpose of the Study:
- To identify novel therapeutic targets for reversing EMT.
- To investigate the role of kinases in maintaining mesenchymal cell properties.
Main Methods:
- Screening a lentiviral kinome shRNA library in MCF10A breast epithelial cells.
- Assessing the impact of kinase knockdown on a 26-gene EMT RNA signature.
- Evaluating the effect of MAPK7 suppression on breast cancer cell migration and metastasis in an orthotopic mouse model.
Main Results:
- Knockdown of multiple kinases, including mitogen-activated protein kinase 7 (MAPK7), induced epithelial markers.
- Suppression of MAPK7 increased E-cadherin (CDH1) expression and inhibited breast cancer cell migration.
- MAPK7 suppression reduced circulating tumor cells and lung metastases in a mouse model.
Conclusions:
- MAPK7 plays a role in maintaining mesenchymal cell properties in cancer.
- Targeting MAPK7 can induce epithelial markers and inhibit tumor cell invasion and metastasis.
- MAPK7 is a potential therapeutic target for reducing cancer invasiveness and metastasis.
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