PMID- 24649138
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211021
IS  - 2049-9450 (Print)
IS  - 2049-9469 (Electronic)
IS  - 2049-9450 (Linking)
VI  - 1
IP  - 1
DP  - 2013 Jan
TI  - Influence of GRPR and BDNF/TrkB signaling on the viability of breast and 
      gynecologic cancer cells.
PG  - 148-152
AB  - Neuropeptide and neurotrophin receptors are increasingly important molecular 
      targets in cancer. Scientific findings indicate that compounds blocking 
      gastrin-releasing peptide receptors (GRPR) or tropomyosin receptor kinase (Trk) 
      receptors are likely to have antiproliferative activities against cancer cells. 
      The present study aimed to demonstrate that, in contrast to previous findings, 
      GRPR activation reduces, whereas its blockade increases the viability of breast, 
      ovarian and cervical cancer cell lines. However, consistent with previous 
      studies, Trk inhibition was demonstrated to reduce the viability of these cells. 
      MCF-7 (breast), OVCAR-3 (ovarian) and HeLa (cervical) human cancer cell lines 
      were treated with GRP, the GRPR antagonists RC-3095 and RC-3940-II, brain-derived 
      neurotrophic factor (BDNF) and the Trk antagonist K252alpha. Cell viability was 
      measured by the MTT assay. Expression of GRPR and BDNF was confirmed with reverse 
      transcription-polymerase chain reaction (RT-PCR). GRP reduced, whereas RC-3940-II 
      enhanced the viability of the three cell lines. Treatment with K252alpha inhibited 
      the viability of the cell lines, while BDNF increased the viability of OVCAR-3 
      cells. The results supported the hypothesis that GRPR and BDNF/TrkB signaling 
      regulates cancer cell viability. Most importantly, these findings are the first 
      to demonstrate that GRPR blockade can stimulate, rather than inhibits the 
      viability of breast and gynecologic cancer cell lines.
FAU - Cornelio, Daniela B
AU  - Cornelio DB
AD  - Cancer Research Laboratory, University Hospital Research Center (CPE-HCPA);
FAU - DE Farias, Caroline B
AU  - DE Farias CB
AD  - Cancer Research Laboratory, University Hospital Research Center (CPE-HCPA);
FAU - Prusch, Debora S
AU  - Prusch DS
AD  - Cancer Research Laboratory, University Hospital Research Center (CPE-HCPA);
FAU - Heinen, Tiago E
AU  - Heinen TE
AD  - Cancer Research Laboratory, University Hospital Research Center (CPE-HCPA);
FAU - Dos Santos, Rafael P
AU  - Dos Santos RP
AD  - Cancer Research Laboratory, University Hospital Research Center (CPE-HCPA);
FAU - Abujamra, Ana L
AU  - Abujamra AL
AD  - Cancer Research Laboratory, University Hospital Research Center (CPE-HCPA);
FAU - Schwartsmann, Gilberto
AU  - Schwartsmann G
AD  - Cancer Research Laboratory, University Hospital Research Center (CPE-HCPA); ; 
      National Institute for Translational Medicine (INCT-TM); ; Department of Internal 
      Medicine, School of Medicine, Federal University of Rio Grande do Sul, Porto 
      Alegre, RS, Brazil.
FAU - Roesler, Rafael
AU  - Roesler R
AD  - Cancer Research Laboratory, University Hospital Research Center (CPE-HCPA);
LA  - eng
PT  - Journal Article
DEP - 20120807
PL  - England
TA  - Mol Clin Oncol
JT  - Molecular and clinical oncology
JID - 101613422
PMC - PMC3956240
OTO - NOTNLM
OT  - brain-derived neurotrophic factor
OT  - cancer cell
OT  - gastrin-releasing peptide receptor
OT  - gynecologic cancer
OT  - tropomyosin receptor kinase B
EDAT- 2013/01/01 00:00
MHDA- 2013/01/01 00:01
PMCR- 2012/08/07
CRDT- 2014/03/21 06:00
PHST- 2012/06/14 00:00 [received]
PHST- 2012/08/01 00:00 [accepted]
PHST- 2014/03/21 06:00 [entrez]
PHST- 2013/01/01 00:00 [pubmed]
PHST- 2013/01/01 00:01 [medline]
PHST- 2012/08/07 00:00 [pmc-release]
AID - mco-01-01-0148 [pii]
AID - 10.3892/mco.2012.7 [doi]
PST - ppublish
SO  - Mol Clin Oncol. 2013 Jan;1(1):148-152. doi: 10.3892/mco.2012.7. Epub 2012 Aug 7.