Enhancement of vascular endothelial growth factor release in long-term drug-treated breast cancer via transient receptor potential channel 5-Ca2+-hypoxia-inducible factor 1 alpha pathway
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AbstractChemotherapy targeting anti-angiogenesis in tumors may have insufficient efficacy, but little is known about the underlying mechanisms. Here, we showed that the Ca2+-permeable channel, TrpC5, is highly expressed in human breast cancer after long-term chemotherapy drug-treatment. It mediates downstream hypoxia-inducible factor 1 alpha accumulation in the nucleus, and then activates the transcription of vascular endothelial growth factor which promotes tumor angiogenesis, leading to a poor chemotherapeutic outcome. We verified this mechanism at both the cellular and xenograft levels. Moreover, in samples from patients, high TrpC5 expression was correlated with enhanced tumor vasculature after chemotherapy. Taken together, our research demonstrated the essential role of TrpC5 in tumor angiogenesis when facing the challenge of chemotherapy and presents a new potential target for overcoming the high vasculature of human breast cancer after chemotherapy. (C) 2015 Elsevier Ltd. All rights reserved.
All Author(s) ListZhu YF, Pan QX, Meng H, Jiang YS, Mao AQ, Wang T, Hua D, Yao XQ, Jin J, Ma X
Journal namePharmacological Research
Year2015
Month3
Day1
Volume Number93
PublisherACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
Pages36 - 42
ISSN1043-6618
LanguagesEnglish-United Kingdom
KeywordsBreast cancer; Hypoxia-inducible factor (HIF); Long-term drug treatment; Transient receptor potential channel 5 (TrpC5); Vascular endothelial growth factor (VEGF)
Web of Science Subject CategoriesPharmacology & Pharmacy

Last updated on 2020-20-09 at 01:42