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Updated: Feb 25, 2026

In vitro Cell Migration and Invasion Assays
Published on: June 1, 2014
AIM1 is an actin-binding protein that suppresses cell migration and micrometastatic dissemination
Michael C Haffner1,2, David M Esopi1, Alcides Chaux2,3
1Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Abstract:
A defining hallmark of primary and metastatic cancers is the migration and invasion of malignant cells. These invasive properties involve altered dynamics of the cytoskeleton and one of its major structural components β-actin. Here we identify AIM1 (absent in melanoma 1) as an actin-binding protein that suppresses pro-invasive properties in benign prostate epithelium. Depletion of AIM1 in prostate epithelial cells increases cytoskeletal remodeling, intracellular traction forces, cell migration and invasion, and anchorage-independent growth. In addition, decreased AIM1 expression results in increased metastatic dissemination in vivo. AIM1 strongly associates with the actin cytoskeleton in prostate epithelial cells in normal tissues, but not in prostate cancers. In addition to a mislocalization of AIM1 from the actin cytoskeleton in invasive cancers, advanced prostate cancers often harbor AIM1 deletion and reduced expression. These findings implicate AIM1 as a key suppressor of invasive phenotypes that becomes dysregulated in primary and metastatic prostate cancer.
Insights
Absent in melanoma 1 (AIM1) suppresses cancer cell invasion by regulating the actin cytoskeleton. Loss of AIM1 promotes prostate cancer cell migration, invasion, and metastasis, indicating its role as a tumor suppressor.
Area of Science:
- Molecular Biology
- Cancer Research
- Cell Biology
Background:
- Cancer cell migration and invasion are hallmarks of primary and metastatic cancers.
- Altered cytoskeletal dynamics, particularly involving β-actin, are crucial for these invasive properties.
Purpose of the Study:
- To identify novel actin-binding proteins that regulate cancer cell invasion.
- To investigate the role of Absent in melanoma 1 (AIM1) in prostate cancer progression.
Main Methods:
- Depletion of AIM1 in prostate epithelial cells.
- Assessment of cytoskeletal remodeling, cell migration, invasion, and anchorage-independent growth.
- In vivo studies to evaluate metastatic dissemination.
- Analysis of AIM1 expression and localization in normal and cancerous prostate tissues.
Main Results:
- AIM1 depletion increased cytoskeletal remodeling, intracellular traction forces, cell migration, invasion, and anchorage-independent growth.
- Reduced AIM1 expression led to increased metastatic dissemination in vivo.
- AIM1 associated with the actin cytoskeleton in normal prostate cells but was mislocalized in prostate cancers.
- Advanced prostate cancers showed AIM1 deletion and reduced expression.
Conclusions:
- AIM1 acts as a suppressor of pro-invasive phenotypes in prostate epithelial cells.
- Dysregulation of AIM1, including mislocalization and reduced expression, is implicated in primary and metastatic prostate cancer.
- AIM1 is a potential therapeutic target for suppressing prostate cancer invasion and metastasis.
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