Influence of GRPR and BDNF/TrkB signaling on the viability of breast and gynecologic cancer cells
Autor(a) principal: | |
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Data de Publicação: | 2013 |
Outros Autores: | , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/194216 |
Resumo: | 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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Cornélio, Daniela BaumannFarias, Caroline Brunetto dePrusch, Débora SchoenfeldHeinen, Tiago EliasSantos, Rafael Pereira dosAbujamra, Ana LúciaSchwartsmann, GilbertoRoesler, Rafael2019-05-14T02:38:19Z20132049-9469http://hdl.handle.net/10183/194216000980277Neuropeptide 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.application/pdfengMolecular and clinical oncology. Londres. Vol. 1, no. 1 (Jan. 2013), p. 148-152Peptídeo liberador de gastrinaReceptores da bombesinaFator neurotrófico derivado do encéfaloNeoplasias da mamaGastrin releasing peptide receptorCancer cellGynecologic cancerTropomyosin receptor kinase BBrain derived neurotrophic factorInfluence of GRPR and BDNF/TrkB signaling on the viability of breast and gynecologic cancer cellsEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT000980277.pdf.txt000980277.pdf.txtExtracted Texttext/plain27631http://www.lume.ufrgs.br/bitstream/10183/194216/2/000980277.pdf.txte9f7c34fa1907289b6fe41c682949bfeMD52ORIGINAL000980277.pdfTexto completo (inglês)application/pdf501718http://www.lume.ufrgs.br/bitstream/10183/194216/1/000980277.pdf2a36193f073add90dabc75871d2542dfMD5110183/1942162019-05-15 02:37:55.693922oai:www.lume.ufrgs.br:10183/194216Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2019-05-15T05:37:55Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
Influence of GRPR and BDNF/TrkB signaling on the viability of breast and gynecologic cancer cells |
title |
Influence of GRPR and BDNF/TrkB signaling on the viability of breast and gynecologic cancer cells |
spellingShingle |
Influence of GRPR and BDNF/TrkB signaling on the viability of breast and gynecologic cancer cells Cornélio, Daniela Baumann Peptídeo liberador de gastrina Receptores da bombesina Fator neurotrófico derivado do encéfalo Neoplasias da mama Gastrin releasing peptide receptor Cancer cell Gynecologic cancer Tropomyosin receptor kinase B Brain derived neurotrophic factor |
title_short |
Influence of GRPR and BDNF/TrkB signaling on the viability of breast and gynecologic cancer cells |
title_full |
Influence of GRPR and BDNF/TrkB signaling on the viability of breast and gynecologic cancer cells |
title_fullStr |
Influence of GRPR and BDNF/TrkB signaling on the viability of breast and gynecologic cancer cells |
title_full_unstemmed |
Influence of GRPR and BDNF/TrkB signaling on the viability of breast and gynecologic cancer cells |
title_sort |
Influence of GRPR and BDNF/TrkB signaling on the viability of breast and gynecologic cancer cells |
author |
Cornélio, Daniela Baumann |
author_facet |
Cornélio, Daniela Baumann Farias, Caroline Brunetto de Prusch, Débora Schoenfeld Heinen, Tiago Elias Santos, Rafael Pereira dos Abujamra, Ana Lúcia Schwartsmann, Gilberto Roesler, Rafael |
author_role |
author |
author2 |
Farias, Caroline Brunetto de Prusch, Débora Schoenfeld Heinen, Tiago Elias Santos, Rafael Pereira dos Abujamra, Ana Lúcia Schwartsmann, Gilberto Roesler, Rafael |
author2_role |
author author author author author author author |
dc.contributor.author.fl_str_mv |
Cornélio, Daniela Baumann Farias, Caroline Brunetto de Prusch, Débora Schoenfeld Heinen, Tiago Elias Santos, Rafael Pereira dos Abujamra, Ana Lúcia Schwartsmann, Gilberto Roesler, Rafael |
dc.subject.por.fl_str_mv |
Peptídeo liberador de gastrina Receptores da bombesina Fator neurotrófico derivado do encéfalo Neoplasias da mama |
topic |
Peptídeo liberador de gastrina Receptores da bombesina Fator neurotrófico derivado do encéfalo Neoplasias da mama Gastrin releasing peptide receptor Cancer cell Gynecologic cancer Tropomyosin receptor kinase B Brain derived neurotrophic factor |
dc.subject.eng.fl_str_mv |
Gastrin releasing peptide receptor Cancer cell Gynecologic cancer Tropomyosin receptor kinase B Brain derived neurotrophic factor |
description |
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. |
publishDate |
2013 |
dc.date.issued.fl_str_mv |
2013 |
dc.date.accessioned.fl_str_mv |
2019-05-14T02:38:19Z |
dc.type.driver.fl_str_mv |
Estrangeiro info:eu-repo/semantics/article |
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info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10183/194216 |
dc.identifier.issn.pt_BR.fl_str_mv |
2049-9469 |
dc.identifier.nrb.pt_BR.fl_str_mv |
000980277 |
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2049-9469 000980277 |
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http://hdl.handle.net/10183/194216 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.pt_BR.fl_str_mv |
Molecular and clinical oncology. Londres. Vol. 1, no. 1 (Jan. 2013), p. 148-152 |
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info:eu-repo/semantics/openAccess |
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openAccess |
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