PMID- 24323291
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20131210
LR  - 20211021
IS  - 2157-9024 (Print)
IS  - 2157-9024 (Electronic)
IS  - 2157-9024 (Linking)
VI  - 2
IP  - 12
DP  - 2013 Dec 9
TI  - Protein tyrosine kinase 6 regulates mammary gland tumorigenesis in mouse models.
PG  - e81
LID - 10.1038/oncsis.2013.43 [doi]
AB  - Protein tyrosine kinase 6 (PTK6, also called BRK) is an intracellular tyrosine 
      kinase expressed in the majority of human breast tumors and breast cancer cell 
      lines, but its expression has not been reported in normal mammary gland. To study 
      functions of PTK6 in vivo, we generated and characterized several transgenic 
      mouse lines with expression of human PTK6 under control of the mouse mammary 
      tumor virus (MMTV) long terminal repeat. Ectopic active PTK6 was detected in 
      luminal epithelial cells of mature transgenic mammary glands. Lines expressing 
      the MMTV-PTK6 transgene exhibited more than a two-fold increase in mammary gland 
      tumor formation compared with nontransgenic control animals. PTK6 activates 
      signal transducer and activator of transcription 3 (STAT3), and active STAT3 was 
      detected in PTK6-positive mammary gland epithelial cells. Endogenous mouse PTK6 
      was not detected in the normal mouse mammary gland, but it was induced in mouse 
      mammary gland tumors of different origin, including spontaneous tumors that 
      developed in control mice, and tumors that formed in PTK6, H-Ras, ERBB2 and PyMT 
      transgenic models. MMTV-PTK6 and MMTV-ERBB2 transgenic mice were crossed to 
      explore crosstalk between PTK6 and ERBB2 signaling in vivo. We found no 
      significant increase in tumor incidence, size or metastasis in ERBB2/PTK6 double 
      transgenic mice. Although we detected increased proliferation in ERBB2/PTK6 
      double transgenic tumors, an increase in apoptosis was also observed. MMTV-PTK6 
      clearly promotes mammary gland tumorigenesis in vivo, but its impact may be 
      underrepresented in our transgenic models because of induction of endogenous PTK6 
      expression.
FAU - Peng, M
AU  - Peng M
AD  - Department of Biochemistry and Molecular Genetics, University of Illinois College 
      of Medicine, Chicago, IL, USA.
FAU - Ball-Kell, S M
AU  - Ball-Kell SM
FAU - Franks, R R
AU  - Franks RR
FAU - Xie, H
AU  - Xie H
FAU - Tyner, A L
AU  - Tyner AL
LA  - eng
GR  - R01 DK044525/DK/NIDDK NIH HHS/United States
GR  - UL1 TR000050/TR/NCATS NIH HHS/United States
PT  - Journal Article
DEP - 20131209
PL  - United States
TA  - Oncogenesis
JT  - Oncogenesis
JID - 101580004
PMC - PMC3940860
EDAT- 2013/12/11 06:00
MHDA- 2013/12/11 06:01
PMCR- 2013/12/01
CRDT- 2013/12/11 06:00
PHST- 2013/09/23 00:00 [received]
PHST- 2013/10/10 00:00 [revised]
PHST- 2013/10/29 00:00 [accepted]
PHST- 2013/12/11 06:00 [entrez]
PHST- 2013/12/11 06:00 [pubmed]
PHST- 2013/12/11 06:01 [medline]
PHST- 2013/12/01 00:00 [pmc-release]
AID - oncsis201343 [pii]
AID - 10.1038/oncsis.2013.43 [doi]
PST - epublish
SO  - Oncogenesis. 2013 Dec 9;2(12):e81. doi: 10.1038/oncsis.2013.43.