ArticleMolecular and clinical oncology2013
Influence of GRPR and BDNF/TrkB signaling on the viability of breast and gynecologic cancer cells.
Article in Molecular and clinical oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- The gastrin-releasing peptide receptor as a potential biomarker for squamous cell carcinoma.Scientific reports · 2025Article
- Role of NTRK Fusion Genes in the Tumor Immune Microenvironment of HPV (+/-) Cervical Cancer.Journal of medical virology · 2025Review
- Gastrin-releasing peptide receptor: a promising new biomarker to identify cervical precursor lesions and cancer.Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia · 2025Article
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- Human gastrin- releasing peptide receptor expression in women with uterine cervix cancer.Frontiers in oncology · 2023Article
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- Neurotrophic receptor tyrosine kinase family members in secretory and non-secretory breast carcinomas.World journal of clinical oncology · 2022Article
- Ovarian BDNF promotes survival, migration, and attachment of tumor precursors originated from p53 mutant fallopian tube epithelial cells.Oncogenesis · 2020Article
- Bombesin related peptides/receptors and their promising therapeutic roles in cancer imaging, targeting and treatment.Expert opinion on therapeutic targets · 2016Review
- Trk inhibition reduces cell proliferation and potentiates the effects of chemotherapeutic agents in Ewing sarcoma.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 K252α. 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 K252α 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.
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