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Epithelial Membrane Protein 2 and β1 integrin signaling regulate APC-mediated processes
Alyssa C Lesko1, Jenifer R Prosperi2
1Department of Biological Science, Harper Cancer Research Institute, University of Notre Dame, United States.
Experimental Cell Research
|November 29, 2016
Summary
Loss of Adenomatous Polyposis Coli (APC) impacts cell polarity and migration via two new pathways: Epithelial Membrane Protein 2 (EMP2) and β1 integrin signaling, independent of Wnt signaling.
Area of Science:
- Cell Biology
- Molecular Biology
- Epithelial Biology
Background:
- Adenomatous Polyposis Coli (APC) is crucial for cell motility, polarity, and epithelial development.
- APC loss in Madin Darby Canine Kidney (MDCK) cells increases cyst size, inverts polarity, and upregulates Epithelial Membrane Protein 2 (EMP2).
Purpose of the Study:
- To elucidate the molecular mechanisms by which APC influences cell polarity and motility.
- To investigate the roles of Epithelial Membrane Protein 2 (EMP2) and β1 integrin in APC-mediated regulation.
Main Methods:
- Utilized 3D in vitro model systems and 2D migration assays.
- Performed EMP2 knockdown in APC-depleted MDCK cells.
- Employed chemical inhibition of β1 integrin and its downstream signaling components (FAK, Src).
Main Results:
- APC loss increases β1 integrin expression and cell migration in MDCK cells.
- APC regulates apical-basal polarity and cyst size via EMP2.
- APC controls cyst size and migration, but not polarity, through β1 integrin signaling.
Conclusions:
- Identified EMP2 as a mediator for APC's regulation of polarity and cyst size.
- Identified β1 integrin signaling as a mediator for APC's regulation of cyst size and migration.
- Discovered two novel, Wnt-independent mechanisms by which APC controls polarity, cyst size, and cell migration.
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