AIM1 is an actin-binding protein that suppresses cell migration and micrometastatic dissemination

Michael C. Haffner, David M. Esopi, Alcides Chaux, Meltem Gürel, Susmita Ghosh, Ajay M. Vaghasia, Harrison Tsai, Kunhwa Kim, Nicole Castagna, Hong Lam, Jessica Hicks, Nicolas Wyhs, Debika Biswal Shinohara, Paula J. Hurley, Brian W. Simons, Edward M. Schaeffer, Tamara L. Lotan, William B. Isaacs, George J. Netto, Angelo M. De Marzo, William G. Nelson, Steven S. An and Srinivasan Yegnasubramanian ()
Additional contact information
Michael C. Haffner: Johns Hopkins University
David M. Esopi: Johns Hopkins University
Alcides Chaux: Johns Hopkins University
Meltem Gürel: Johns Hopkins University
Susmita Ghosh: Johns Hopkins University
Ajay M. Vaghasia: Johns Hopkins University
Harrison Tsai: Johns Hopkins University
Kunhwa Kim: Johns Hopkins University
Nicole Castagna: Johns Hopkins University
Hong Lam: Johns Hopkins University
Jessica Hicks: Johns Hopkins University
Nicolas Wyhs: Johns Hopkins University
Debika Biswal Shinohara: Johns Hopkins University
Paula J. Hurley: Johns Hopkins University
Brian W. Simons: Johns Hopkins University
Edward M. Schaeffer: Johns Hopkins University
Tamara L. Lotan: Johns Hopkins University
William B. Isaacs: Johns Hopkins University
George J. Netto: Johns Hopkins University
Angelo M. De Marzo: Johns Hopkins University
William G. Nelson: Johns Hopkins University
Steven S. An: Johns Hopkins University
Srinivasan Yegnasubramanian: Johns Hopkins University

Nature Communications, 2017, vol. 8, issue 1, 1-17

Abstract: 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.

Date: 2017
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DOI: 10.1038/s41467-017-00084-8

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