PDLIM4, an actin binding protein, suppresses prostate cancer cell growth

Donkena Krishna Vanaja, Michael E. Grossmann, John C. Cheville, Mozammel H. Gazi, Aiyu Gong, Jin San Zhang, Katalin Ajtai, Thomas P. Burghardt, Charles Y.F. Young

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

We investigated the molecular function of PDLIM4 in prostate cancer cells. PDLIM4 mRNA and protein-expression levels were reduced in LNCaP, LAPC4, DU145, CWR22, and PC3 prostate cancer cells. The re-expression of PDLIM4 in prostate cancer cells has significantly reduced the cell growth and clonogenicity with G1 phase of cell-cycle arrest. We have shown the direct interaction of PDLIM4 with F-actin. Restoration of PDLIM4 expression resulted in reduction of tumor growth in xenografts. These results suggest that PDLIM4 may function as a tumor suppressor, involved in the control of cell proliferation by associating with actin in prostate cancer cells.

Original languageEnglish (US)
Pages (from-to)264-272
Number of pages9
JournalCancer Investigation
Volume27
Issue number3
DOIs
StatePublished - Mar 2009

Bibliographical note

Funding Information:
Keywords: Prostate cancer, Tumor suppressor gene, LIM domain protein, Cell growth, Actin cytoskeleton This work was supported in part by NIH grants R01 AR049277 and CA70892. Dr. Vanaja DK and Dr. Grossman ME contributed equally to this study. Correspondence to: Charles Y. F. Young, Ph.D. Professor Department of Urology and Biochemistry and Molecular Biology Guggenheim 520 C, Mayo Clinic College of Medicine 200 1st street S.W. Rochester, MN 55905, USA email: youngc@mayo.edu

Keywords

  • Actin cytoskeleton
  • Cell growth
  • LIM domain protein
  • Prostate cancer
  • Tumor suppressor gene

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