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Trop2 expression contributes to tumor pathogenesis by activating the ERK MAPK pathway.
Rafael Cubas1, Sheng Zhang, Min Li
1Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, USA.
Molecular Cancer
|September 23, 2010
Summary
Trop2 (Trophoblast cell-surface antigen 2) promotes cancer growth and metastasis. This study reveals Trop2 activates ERK signaling, impacting cell cycle regulators and highlighting Trop2 as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Trop2 (Trophoblast cell-surface antigen 2) is a cell-surface glycoprotein.
- Overexpressed in various epithelial carcinomas, linked to tumor aggressiveness and poor patient survival.
- Signaling mechanisms of Trop2 remain largely unknown.
Purpose of the Study:
- Investigate the effects of murine Trop2 (mTrop2) on tumor cell functions.
- Elucidate signaling pathways activated by Trop2.
Main Methods:
- In vitro assays assessing proliferation, migration, foci formation, and anchorage-independent growth.
- Murine models for subcutaneous and orthotopic pancreatic cancer.
- Analysis of signaling pathways including ERK, cyclin D1, cyclin E, and p27.
- Experiments with human pancreatic and colorectal cancer cells.
Main Results:
- mTrop2 expression enhanced tumor cell proliferation, migration, and growth in vivo.
- Increased liver metastasis observed in murine models.
- mTrop2 upregulated phosphorylated ERK1/2, leading to increased cyclin D1/E and decreased p27, promoting cell cycle progression.
- ERK activation confirmed in human cancer cells overexpressing Trop2.
Conclusions:
- mTrop2 expression drives pathogenic effects in cancer cells.
- Trop2 targeting is crucial for cancer therapy.
- Identified a novel Trop2-activated signaling pathway impacting cancer cell growth and survival.
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