Direct targeting of Sec23a by miR-200s influences cancer cell secretome and promotes metastatic colonization
- 1Department of Molecular Biology, Princeton University, Princeton, New Jersey, USA.
- 0Department of Molecular Biology, Princeton University, Princeton, New Jersey, USA.
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View abstract on PubMed
Summary
This summary is machine-generated.MicroRNAs miR-200s promote breast cancer metastasis beyond regulating E-cadherin. They enhance metastatic colonization by targeting Sec23a, influencing metastasis-suppressive protein secretion.
Area Of Science
- Oncology
- Molecular Biology
- Genetics
Background
- The miR-200 family's role in epithelial-mesenchymal transition (EMT) and E-cadherin regulation is known.
- Their specific impact on metastatic colonization in breast cancer remains debated.
Purpose Of The Study
- To investigate the role of miR-200s in breast cancer metastasis.
- To explore miR-200s' pro-metastatic functions beyond E-cadherin regulation.
Main Methods
- Utilized clinical and experimental breast cancer metastasis models.
- Performed genomic and proteomic analyses.
- Investigated direct targeting of Sec23a by miR-200s and its downstream effects.
Main Results
- miR-200 overexpression correlates with increased metastasis risk and promotes colonization in mouse models.
- miR-200s induce global gene expression changes towards highly metastatic phenotypes.
- miR-200s target Sec23a, reducing secretion of metastasis-suppressive proteins like Igfbp4 and Tinagl1.
Conclusions
- miR-200s play a significant pro-metastatic role in breast cancer.
- This role extends beyond E-cadherin regulation, involving Sec23a-mediated secretome modulation.
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