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Command and control: regulatory pathways controlling invasive behavior of the border cells
1Department of Biological Chemistry, Johns Hopkins University School of Medicine, 725 North Wolfe Street, 21205-2185, Baltimore, MD, USA. dmontell@jhmi.edu
Mechanisms of Development
|June 29, 2001
Summary
Cancer cell invasiveness mirrors developmental cell migration. Drosophila border cell migration requires C/EBP and ecdysone receptor pathways, revealing steroid hormone regulation of cell motility.
Area of Science:
- Developmental Biology
- Cell Biology
- Molecular Biology
Background:
- Cancer cell invasiveness shares similarities with normal developmental cell migration.
- Drosophila border cells provide a model system for studying cell invasion during development.
Purpose of the Study:
- To investigate the genetic regulatory pathways controlling Drosophila border cell migration.
- To understand the role of transcriptional regulation and hormonal signaling in cell motility.
Main Methods:
- Genetic screening approaches in Drosophila.
- Analysis of gene expression and protein localization (e.g., DE-cadherin, FAK).
- Investigating the function of the slbo gene (Drosophila C/EBP) and the Taiman (TAI) co-activator for the ecdysone receptor.
Main Results:
- Border cell migration requires the integration of at least two transcriptional regulatory pathways: one involving slbo (Drosophila C/EBP) and another involving the ecdysone receptor and Taiman (TAI).
- The C/EBP pathway upregulates motility-related proteins like DE-cadherin and FAK.
- The ecdysone pathway, influenced by nutrition, regulates the localization of C/EBP targets and is crucial for cell migration, as evidenced by migration defects in tai mutants.
Conclusions:
- Drosophila border cell migration is controlled by a differentiation program (C/EBP) and a hormonal signal (ecdysone).
- Steroid hormones can directly regulate cell motility, independent of proliferation.
- These findings offer insights into the metastatic effects of steroid hormones in cancer and the action of antagonists like tamoxifen.
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