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

Author

Listed:
  • Michael C. Haffner

    (Johns Hopkins University
    Johns Hopkins University)

  • David M. Esopi

    (Johns Hopkins University)

  • Alcides Chaux

    (Johns Hopkins University
    Norte 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
    Johns Hopkins University)

  • Brian W. Simons

    (Johns Hopkins University)

  • Edward M. Schaeffer

    (Johns Hopkins University
    Johns Hopkins University
    Johns Hopkins University)

  • Tamara L. Lotan

    (Johns Hopkins University)

  • William B. Isaacs

    (Johns Hopkins University
    Johns Hopkins University)

  • George J. Netto

    (Johns Hopkins University
    Johns Hopkins University
    Johns Hopkins University)

  • Angelo M. De Marzo

    (Johns Hopkins University
    Johns Hopkins University
    Johns Hopkins University)

  • William G. Nelson

    (Johns Hopkins University
    Johns Hopkins University
    Johns Hopkins University)

  • Steven S. An

    (Johns Hopkins University
    Johns Hopkins University
    Johns Hopkins University)

  • Srinivasan Yegnasubramanian

    (Johns Hopkins University
    Johns Hopkins University
    Johns Hopkins University
    Johns Hopkins University)

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.

Suggested Citation

  • 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 , 2017. "AIM1 is an actin-binding protein that suppresses cell migration and micrometastatic dissemination," Nature Communications, Nature, vol. 8(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00084-8
    DOI: 10.1038/s41467-017-00084-8
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