Journal
CANCER INVESTIGATION
Volume 27, Issue 3, Pages 264-272Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/07357900802406319
Keywords
Prostate cancer; Tumor suppressor gene; LIM domain protein; Cell growth; Actin cytoskeleton
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Funding
- NIH [R01 AR049277, CA70892]
- NATIONAL CANCER INSTITUTE [R01CA070892] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR049277] Funding Source: NIH RePORTER
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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.
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