Cargando…
SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1
Growth factor receptor tyrosine kinase (RTK) pathway activation is a key mechanism for mediating cancer growth, survival, and treatment resistance. Cognate ligands play crucial roles in autocrine or paracrine stimulation of these RTK pathways. Here, we show SEMA3C drives activation of multiple RTKs...
Autores principales: | , , , , , , , , , , , , , , , , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5801490/ https://www.ncbi.nlm.nih.gov/pubmed/29348142 http://dx.doi.org/10.15252/emmm.201707689 |
_version_ | 1783298358202335232 |
---|---|
author | Peacock, James W Takeuchi, Ario Hayashi, Norihiro Liu, Liangliang Tam, Kevin J Al Nakouzi, Nader Khazamipour, Nastaran Tombe, Tabitha Dejima, Takashi Lee, Kevin CK Shiota, Masaki Thaper, Daksh Lee, Wilson CW Hui, Daniel HF Kuruma, Hidetoshi Ivanova, Larissa Yenki, Parvin Jiao, Ivy ZF Khosravi, Shahram Mui, Alice L‐F Fazli, Ladan Zoubeidi, Amina Daugaard, Mads Gleave, Martin E Ong, Christopher J |
author_facet | Peacock, James W Takeuchi, Ario Hayashi, Norihiro Liu, Liangliang Tam, Kevin J Al Nakouzi, Nader Khazamipour, Nastaran Tombe, Tabitha Dejima, Takashi Lee, Kevin CK Shiota, Masaki Thaper, Daksh Lee, Wilson CW Hui, Daniel HF Kuruma, Hidetoshi Ivanova, Larissa Yenki, Parvin Jiao, Ivy ZF Khosravi, Shahram Mui, Alice L‐F Fazli, Ladan Zoubeidi, Amina Daugaard, Mads Gleave, Martin E Ong, Christopher J |
author_sort | Peacock, James W |
collection | PubMed |
description | Growth factor receptor tyrosine kinase (RTK) pathway activation is a key mechanism for mediating cancer growth, survival, and treatment resistance. Cognate ligands play crucial roles in autocrine or paracrine stimulation of these RTK pathways. Here, we show SEMA3C drives activation of multiple RTKs including EGFR, ErbB2, and MET in a cognate ligand‐independent manner via Plexin B1. SEMA3C expression levels increase in castration‐resistant prostate cancer (CRPC), where it functions to promote cancer cell growth and resistance to androgen receptor pathway inhibition. SEMA3C inhibition delays CRPC and enzalutamide‐resistant progression. Plexin B1 sema domain‐containing:Fc fusion proteins suppress RTK signaling and cell growth and inhibit CRPC progression of LNCaP xenografts post‐castration in vivo. SEMA3C inhibition represents a novel therapeutic strategy for treatment of advanced prostate cancer. |
format | Online Article Text |
id | pubmed-5801490 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-58014902018-02-15 SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1 Peacock, James W Takeuchi, Ario Hayashi, Norihiro Liu, Liangliang Tam, Kevin J Al Nakouzi, Nader Khazamipour, Nastaran Tombe, Tabitha Dejima, Takashi Lee, Kevin CK Shiota, Masaki Thaper, Daksh Lee, Wilson CW Hui, Daniel HF Kuruma, Hidetoshi Ivanova, Larissa Yenki, Parvin Jiao, Ivy ZF Khosravi, Shahram Mui, Alice L‐F Fazli, Ladan Zoubeidi, Amina Daugaard, Mads Gleave, Martin E Ong, Christopher J EMBO Mol Med Research Articles Growth factor receptor tyrosine kinase (RTK) pathway activation is a key mechanism for mediating cancer growth, survival, and treatment resistance. Cognate ligands play crucial roles in autocrine or paracrine stimulation of these RTK pathways. Here, we show SEMA3C drives activation of multiple RTKs including EGFR, ErbB2, and MET in a cognate ligand‐independent manner via Plexin B1. SEMA3C expression levels increase in castration‐resistant prostate cancer (CRPC), where it functions to promote cancer cell growth and resistance to androgen receptor pathway inhibition. SEMA3C inhibition delays CRPC and enzalutamide‐resistant progression. Plexin B1 sema domain‐containing:Fc fusion proteins suppress RTK signaling and cell growth and inhibit CRPC progression of LNCaP xenografts post‐castration in vivo. SEMA3C inhibition represents a novel therapeutic strategy for treatment of advanced prostate cancer. John Wiley and Sons Inc. 2018-01-18 2018-02 /pmc/articles/PMC5801490/ /pubmed/29348142 http://dx.doi.org/10.15252/emmm.201707689 Text en © 2018 The Authors. Published under the terms of the CC BY 4.0 license This is an open access article under the terms of the Creative Commons Attribution 4.0 (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Peacock, James W Takeuchi, Ario Hayashi, Norihiro Liu, Liangliang Tam, Kevin J Al Nakouzi, Nader Khazamipour, Nastaran Tombe, Tabitha Dejima, Takashi Lee, Kevin CK Shiota, Masaki Thaper, Daksh Lee, Wilson CW Hui, Daniel HF Kuruma, Hidetoshi Ivanova, Larissa Yenki, Parvin Jiao, Ivy ZF Khosravi, Shahram Mui, Alice L‐F Fazli, Ladan Zoubeidi, Amina Daugaard, Mads Gleave, Martin E Ong, Christopher J SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1 |
title |
SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1 |
title_full |
SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1 |
title_fullStr |
SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1 |
title_full_unstemmed |
SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1 |
title_short |
SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1 |
title_sort | sema3c drives cancer growth by transactivating multiple receptor tyrosine kinases via plexin b1 |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5801490/ https://www.ncbi.nlm.nih.gov/pubmed/29348142 http://dx.doi.org/10.15252/emmm.201707689 |
work_keys_str_mv | AT peacockjamesw sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT takeuchiario sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT hayashinorihiro sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT liuliangliang sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT tamkevinj sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT alnakouzinader sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT khazamipournastaran sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT tombetabitha sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT dejimatakashi sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT leekevinck sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT shiotamasaki sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT thaperdaksh sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT leewilsoncw sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT huidanielhf sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT kurumahidetoshi sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT ivanovalarissa sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT yenkiparvin sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT jiaoivyzf sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT khosravishahram sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT muialicelf sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT fazliladan sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT zoubeidiamina sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT daugaardmads sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT gleavemartine sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 AT ongchristopherj sema3cdrivescancergrowthbytransactivatingmultiplereceptortyrosinekinasesviaplexinb1 |