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
Publication in refereed journal

香港中文大學研究人員

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摘要Chemotherapy 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.
著者Zhu YF, Pan QX, Meng H, Jiang YS, Mao AQ, Wang T, Hua D, Yao XQ, Jin J, Ma X
期刊名稱Pharmacological Research
出版年份2015
月份3
日期1
卷號93
出版社ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
頁次36 - 42
國際標準期刊號1043-6618
語言英式英語
關鍵詞Breast cancer; Hypoxia-inducible factor (HIF); Long-term drug treatment; Transient receptor potential channel 5 (TrpC5); Vascular endothelial growth factor (VEGF)
Web of Science 學科類別Pharmacology & Pharmacy

上次更新時間 2020-22-10 於 01:48