Posttranscriptional suppression of proto-oncogene c-fms expression by vigilin in breast cancer

Ho Hyung Woo, Xiaofang Yi, Tiffany Lamb, Ina Menzl, Terri Baker, David J. Shapiro, Setsuko K Chambers

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

cis-acting elements found in 3′-untranslated regions (UTRs) are regulatory signals determining mRNA stability and translational efficiency. By binding a novel non-AU-rich 69-nucleotide (nt) c-fms 3′ UTR sequence, we previously identified HuR as a promoter of c-fms proto-oncogene mRNA. We now identify the 69-nt c-fms mRNA 3′ UTR sequence as a cellular vigilin target through which vigilin inhibits the expression of c-fms mRNA and protein. Altering association of either vigilin or HuR with c-fms mRNA in vivo reciprocally affected mRNA association with the other protein. Mechanistic studies show that vigilin decreased c-fms mRNA stability. Furthermore, vigilin inhibited c-fms translation. Vigilin suppresses while HuR encourages cellular motility and invasion of breast cancer cells. In summary, we identified a competition for binding the 69-nt sequence, through which vigilin and HuR exert opposing effects on c-fms expression, suggesting a role for vigilin in suppression of breast cancer progression.

Original languageEnglish (US)
Pages (from-to)215-225
Number of pages11
JournalMolecular and Cellular Biology
Volume31
Issue number1
DOIs
StatePublished - Jan 2011

Fingerprint

fms Genes
Breast Neoplasms
3' Untranslated Regions
Messenger RNA
RNA Stability
Nucleotides
Macrophage Colony-Stimulating Factor Receptors
high density lipoprotein binding protein

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Cite this

Posttranscriptional suppression of proto-oncogene c-fms expression by vigilin in breast cancer. / Woo, Ho Hyung; Yi, Xiaofang; Lamb, Tiffany; Menzl, Ina; Baker, Terri; Shapiro, David J.; Chambers, Setsuko K.

In: Molecular and Cellular Biology, Vol. 31, No. 1, 01.2011, p. 215-225.

Research output: Contribution to journalArticle

Woo, Ho Hyung ; Yi, Xiaofang ; Lamb, Tiffany ; Menzl, Ina ; Baker, Terri ; Shapiro, David J. ; Chambers, Setsuko K. / Posttranscriptional suppression of proto-oncogene c-fms expression by vigilin in breast cancer. In: Molecular and Cellular Biology. 2011 ; Vol. 31, No. 1. pp. 215-225.
@article{d4bed01bf0c84e059e3182455876ffe6,
title = "Posttranscriptional suppression of proto-oncogene c-fms expression by vigilin in breast cancer",
abstract = "cis-acting elements found in 3′-untranslated regions (UTRs) are regulatory signals determining mRNA stability and translational efficiency. By binding a novel non-AU-rich 69-nucleotide (nt) c-fms 3′ UTR sequence, we previously identified HuR as a promoter of c-fms proto-oncogene mRNA. We now identify the 69-nt c-fms mRNA 3′ UTR sequence as a cellular vigilin target through which vigilin inhibits the expression of c-fms mRNA and protein. Altering association of either vigilin or HuR with c-fms mRNA in vivo reciprocally affected mRNA association with the other protein. Mechanistic studies show that vigilin decreased c-fms mRNA stability. Furthermore, vigilin inhibited c-fms translation. Vigilin suppresses while HuR encourages cellular motility and invasion of breast cancer cells. In summary, we identified a competition for binding the 69-nt sequence, through which vigilin and HuR exert opposing effects on c-fms expression, suggesting a role for vigilin in suppression of breast cancer progression.",
author = "Woo, {Ho Hyung} and Xiaofang Yi and Tiffany Lamb and Ina Menzl and Terri Baker and Shapiro, {David J.} and Chambers, {Setsuko K}",
year = "2011",
month = "1",
doi = "10.1128/MCB.01031-10",
language = "English (US)",
volume = "31",
pages = "215--225",
journal = "Molecular and Cellular Biology",
issn = "0270-7306",
publisher = "American Society for Microbiology",
number = "1",

}

TY - JOUR

T1 - Posttranscriptional suppression of proto-oncogene c-fms expression by vigilin in breast cancer

AU - Woo, Ho Hyung

AU - Yi, Xiaofang

AU - Lamb, Tiffany

AU - Menzl, Ina

AU - Baker, Terri

AU - Shapiro, David J.

AU - Chambers, Setsuko K

PY - 2011/1

Y1 - 2011/1

N2 - cis-acting elements found in 3′-untranslated regions (UTRs) are regulatory signals determining mRNA stability and translational efficiency. By binding a novel non-AU-rich 69-nucleotide (nt) c-fms 3′ UTR sequence, we previously identified HuR as a promoter of c-fms proto-oncogene mRNA. We now identify the 69-nt c-fms mRNA 3′ UTR sequence as a cellular vigilin target through which vigilin inhibits the expression of c-fms mRNA and protein. Altering association of either vigilin or HuR with c-fms mRNA in vivo reciprocally affected mRNA association with the other protein. Mechanistic studies show that vigilin decreased c-fms mRNA stability. Furthermore, vigilin inhibited c-fms translation. Vigilin suppresses while HuR encourages cellular motility and invasion of breast cancer cells. In summary, we identified a competition for binding the 69-nt sequence, through which vigilin and HuR exert opposing effects on c-fms expression, suggesting a role for vigilin in suppression of breast cancer progression.

AB - cis-acting elements found in 3′-untranslated regions (UTRs) are regulatory signals determining mRNA stability and translational efficiency. By binding a novel non-AU-rich 69-nucleotide (nt) c-fms 3′ UTR sequence, we previously identified HuR as a promoter of c-fms proto-oncogene mRNA. We now identify the 69-nt c-fms mRNA 3′ UTR sequence as a cellular vigilin target through which vigilin inhibits the expression of c-fms mRNA and protein. Altering association of either vigilin or HuR with c-fms mRNA in vivo reciprocally affected mRNA association with the other protein. Mechanistic studies show that vigilin decreased c-fms mRNA stability. Furthermore, vigilin inhibited c-fms translation. Vigilin suppresses while HuR encourages cellular motility and invasion of breast cancer cells. In summary, we identified a competition for binding the 69-nt sequence, through which vigilin and HuR exert opposing effects on c-fms expression, suggesting a role for vigilin in suppression of breast cancer progression.

UR - http://www.scopus.com/inward/record.url?scp=78751695662&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78751695662&partnerID=8YFLogxK

U2 - 10.1128/MCB.01031-10

DO - 10.1128/MCB.01031-10

M3 - Article

C2 - 20974809

AN - SCOPUS:78751695662

VL - 31

SP - 215

EP - 225

JO - Molecular and Cellular Biology

JF - Molecular and Cellular Biology

SN - 0270-7306

IS - 1

ER -