PMID- 10565303
OWN - NLM
STAT- MEDLINE
DCOM- 19991207
LR  - 20191210
IS  - 0165-4608 (Print)
IS  - 0165-4608 (Linking)
VI  - 115
IP  - 1
DP  - 1999 Nov
TI  - Loss of heterozygosity on 8p in prostate cancer implicates a role for dematin in 
      tumor progression.
PG  - 65-9
AB  - Dematin is a cytoskeletal protein that bundles actin filaments in a
      phosphorylation-dependent manner. The primary structure of dematin is organized
      into an N-terminal core domain of unknown function and a C-terminal domain that
      is homologous to the "headpiece" domain of villin. We have previously localized
      the dematin gene on human chromosome 8p21.1, a region distal to the ankyrin locus
      for hereditary spherocytosis. Radiation hybrid mapping now places dematin between
      D8S258 and D8S137, two microsatellite markers frequently deleted in prostate
      cancer. The 8p21.1 region is also deleted in prostate, breast, colon, and bladder
      cancers, suggesting the presence of a tumor suppressor gene(s). Using
      laser-capture microdissection technique and fluorescence in situ hybridization
      (FISH), we demonstrate loss of heterozygosity (LOH) of the dematin gene in a
      majority of chromosomal region 8p21-linked prostate tumors. One allele of dematin
      was also deleted in the established prostate adenocarcinoma cell line PC-3, which
      displays a classic oncogenic phenotype. Overexpression of wild-type dematin in
      PC-3 cells resulted in the restoration of a more polarized, epithelial-like
      phenotype. Conversely, the heterologous expression of dominant negative mutants
      of dematin perturbed normal cell morphology of NIH 3T3 fibroblasts. These results
      suggest a biological function of dematin in the regulation of cell shape, with
      implications in the pathobiology of prostate tumorigenesis.
FAU - Lutchman, M
AU  - Lutchman M
AD  - Section of Hematology/Oncology Research, St. Elizabeth's Medical Center, Tufts
      University School of Medicine, Boston, MA 02135, USA.
FAU - Pack, S
AU  - Pack S
FAU - Kim, A C
AU  - Kim AC
FAU - Azim, A
AU  - Azim A
FAU - Emmert-Buck, M
AU  - Emmert-Buck M
FAU - van Huffel, C
AU  - van Huffel C
FAU - Zhuang, Z
AU  - Zhuang Z
FAU - Chishti, A H
AU  - Chishti AH
LA  - eng
GR  - HL51445/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Cancer Genet Cytogenet
JT  - Cancer genetics and cytogenetics
JID - 7909240
RN  - 0 (Blood Proteins)
RN  - 0 (Cytoskeletal Proteins)
RN  - 0 (DMTN protein, human)
RN  - 0 (DNA, Antisense)
RN  - 0 (Dmtn protein, mouse)
RN  - 0 (Microfilament Proteins)
RN  - 0 (Phosphoproteins)
SB  - IM
MH  - 3T3 Cells
MH  - Animals
MH  - Blood Proteins/genetics/*physiology
MH  - *Chromosomes, Human, Pair 8
MH  - Cytoplasm/metabolism
MH  - Cytoskeletal Proteins
MH  - DNA, Antisense/metabolism
MH  - Epithelium/metabolism
MH  - Humans
MH  - *Loss of Heterozygosity
MH  - Male
MH  - Mice
MH  - Microfilament Proteins
MH  - Models, Genetic
MH  - Phenotype
MH  - *Phosphoproteins
MH  - Physical Chromosome Mapping
MH  - Prostate/metabolism
MH  - Prostatic Neoplasms/*genetics
MH  - Tumor Cells, Cultured
EDAT- 1999/11/24 00:00
MHDA- 1999/11/24 00:01
CRDT- 1999/11/24 00:00
PHST- 1999/11/24 00:00 [pubmed]
PHST- 1999/11/24 00:01 [medline]
PHST- 1999/11/24 00:00 [entrez]
AID - S0165460899000813 [pii]
AID - 10.1016/s0165-4608(99)00081-3 [doi]
PST - ppublish
SO  - Cancer Genet Cytogenet. 1999 Nov;115(1):65-9. doi: 10.1016/s0165-4608(99)00081-3.