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A Proximal Culture Method to Study Paracrine Signaling Between Cells
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Homeostatic Signaling by Cell-Cell Junctions and Its Dysregulation during Cancer Progression.
Yang Yu1, Randolph C Elble2,3
1Department of Nature Medicine, Tianjin Medical University School of Pharmacy, Tianjin 300070, China. yuyang@tmu.edu.cn.
Journal of Clinical Medicine
|February 23, 2016
Summary
Epithelial-to-mesenchymal transition (EMT) drives cancer metastasis and therapy resistance. Cell-cell junctions suppress EMT, but their role in cancer is complex. This review explores junctional signaling to inhibit EMT in cancer therapy.
Area of Science:
- Cell Biology
- Cancer Biology
- Developmental Biology
Background:
- Epithelial-to-mesenchymal transition (EMT) is crucial for development and repair but is hijacked by cancer cells for metastasis and therapy resistance.
- EMT also confers stem-like properties, enhancing the colonization of distant organs.
- Cell-cell junctions normally maintain epithelial quiescence and suppress EMT.
Purpose of the Study:
- To review the role of cell-cell junctions in suppressing EMT.
- To discuss conflicting data on junctional signaling in cancer and recent resolutions.
- To explore strategies for inhibiting EMT.
Main Methods:
- Literature review focusing on cell-cell junctions and EMT.
- Analysis of data from breast cancer and other relevant organ sites.
- Evaluation of current and potential EMT inhibition strategies.
Main Results:
- Cell-cell junctions play a critical role in suppressing EMT and maintaining epithelial integrity.
- Junctional signaling in cancer presents complex and sometimes conflicting evidence.
- Recent developments are helping to resolve these conflicts regarding junctional roles.
Conclusions:
- Targeting cell-cell junctions offers potential therapeutic strategies to inhibit EMT.
- Understanding junctional signaling is key to overcoming EMT-driven metastasis and therapy resistance.
- Further research into resolving conflicting data can lead to novel anti-cancer treatments.
Keywords:
E-cadherinEMTPLEKHA7adherens junctionsbreast cancercancer stem cellsclaudinsdisseminationhuman mammary epithelial cellsmiR30btight junctionsMore Related Videos
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