PMID- 17121430
OWN - NLM
STAT- MEDLINE
DCOM- 20070206
LR  - 20170214
IS  - 1533-0346 (Print)
IS  - 1533-0338 (Linking)
VI  - 5
IP  - 6
DP  - 2006 Dec
TI  - Dissection of signaling pathways in fourteen breast cancer cell lines using 
      reverse-phase protein lysate microarray.
PG  - 543-51
AB  - Signal transduction pathways play a crucial role in breast cancer development, 
      progression, and response to different therapies. A major problem in breast 
      cancer therapy is the heterogeneity among different tumor types and cell lines 
      commonly used in preclinical studies. To characterize the signaling pathways of 
      some of the commonly used breast cancer cell lines and dissect the relationship 
      among a number of pathways and some key genetic and molecular events in breast 
      cancer development, such as p53 mutation, ErbB2 expression, and estrogen receptor 
      (ER)/progesterone receptor (PR) status, we performed pathway profiling of 14 
      breast cancer cell lines by measuring the expression and phosphorylation status 
      of 40 different cell signaling proteins with 53 specific antibodies using a 
      protein lysate array. Cluster analysis of the expression data showed that there 
      was close clustering of phosphatidylinositol 3-kinase, Akt, mammalian target of 
      rapamycin (mTOR), Src, and platelet-derived growth factor receptor beta 
      (PDGFRbeta) in all of the cell lines. The most differentially expressed proteins 
      between ER- and PR-positive and ER- and PR-negative breast cells were mTOR, Akt 
      (pThr308), PDGFRbeta, PDGFRbeta (pTyr751), panSrc, Akt (pSer473), insulin-like 
      growth factor-binding protein 5 (IGFBP5), Src (pTyr418), mTOR (pSer2448), and 
      IGFBP2. Many apoptotic proteins, such as apoptosis-inducing factor, IGFBP3, bad, 
      bax, and cleaved caspase 9, were overexpressed in mutant p53-carrying breast 
      cancer cells. Hexokinase isoenzyme 1, ND2, and c-kit were the most differentially 
      expressed proteins in high and low ErbB2-expressing breast cancer cells. This 
      study demonstrated that ER/PR status, ErbB2 expression, and p53 status are major 
      molecules that impact downstream signaling pathways.
FAU - Akkiprik, M
AU  - Akkiprik M
AD  - Department of Pathology, Unit 85, The University of Texas, M. D. Anderson Cancer 
      Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
FAU - Nicorici, D
AU  - Nicorici D
FAU - Cogdell, D
AU  - Cogdell D
FAU - Jia, Y J
AU  - Jia YJ
FAU - Hategan, A
AU  - Hategan A
FAU - Tabus, I
AU  - Tabus I
FAU - Yli-Harja, O
AU  - Yli-Harja O
FAU - Y, D
AU  - Y D
FAU - Sahin, A
AU  - Sahin A
FAU - Zhang, W
AU  - Zhang W
LA  - eng
GR  - CA-16672/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Technol Cancer Res Treat
JT  - Technology in cancer research & treatment
JID - 101140941
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Phosphoproteins)
SB  - IM
MH  - Biomarkers, Tumor/*metabolism
MH  - Breast Neoplasms/*metabolism/pathology
MH  - Cell Line, Tumor
MH  - Female
MH  - Humans
MH  - Phosphoproteins/metabolism
MH  - Protein Array Analysis
MH  - *Signal Transduction
EDAT- 2006/11/24 09:00
MHDA- 2007/02/07 09:00
CRDT- 2006/11/24 09:00
PHST- 2006/11/24 09:00 [pubmed]
PHST- 2007/02/07 09:00 [medline]
PHST- 2006/11/24 09:00 [entrez]
AID - d=3025&c=4218&p=15389&do=detail [pii]
AID - 10.1177/153303460600500601 [doi]
PST - ppublish
SO  - Technol Cancer Res Treat. 2006 Dec;5(6):543-51. doi: 10.1177/153303460600500601.