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Betulinic acid suppresses breast cancer aerobic glycolysis via caveolin-1/NF-κB/c-Myc pathway

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机构: [1]School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou, Guangdong, China [2]Integrative Research Laboratory of Breast Cancer, Discipline of Integrated Chinese and Western Medicine, the Research Center of Integrative Medicine, School of Basic Medical Sciences & the Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China [3]Guangdong Provincial Key Laboratory of Clinical Research on Traditional Chinese Medicine Syndrome, Guangdong Provincial Academy of Chinese Medical Sciences, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, Guangdong, China [4]Post-doctoral Research Center, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China [5]School of Pharmacy, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China
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关键词: Betulinic acid Aerobic glycolysis Caveolin-1 NF-kappa B/c-Myc Breast cancer

摘要:
Emerging evidence has suggested that targeting glycolysis may be a promising strategy for cancer treatment. Betulinic acid (BA) is a natural pentacyclic terpene that has been reported to be active in inhibiting various malignancies. Here, we showed that BA could inhibit aerobic glycolysis activity in breast cancer cell lines MCF-7 and MDA-MB-231 by hampering lactate production, glucose uptake and extracellular acidification rate (ECAR), as well as suppressing aerobic glycolysis-related proteins including c-Myc, lactate dehydrogenase A (LDH-A) and p-PDK1/PDK1 (pyruvate dehydrogenase kinase 1). Mechanistic studies validated Caveolin-1 (Cav-1) as one of key targets of BA in suppressing aerobic glycolysis, as BA administration resulted in Cav-1 upregulation, whereas silencing Cav-1 abrogated the inhibitory effect of BA on aerobic glycolysis. Further investigations demonstrated that BA suppressed aerobic glycolysis in breast cancer cells by regulating the Cav-1/NF-kappa B/c-Myc pathway. More meaningfully, BA significantly inhibited breast cancer growth and glycolytic activity in both the transgenic MMTV-PyVT+/- breast cancer spontaneous model and the zebrafish breast cancer xenotransplantation model without any detectable side effects in vivo. Taken together, our study sheds novel insights into BA as a promising candidate drug for suppressing aerobic glycolysis, highlighting Cav-1 as a potential molecular target of BA and aerobic glycolysis regulation.

基金:

基金编号: 81703749 81703764 81573651 81873306 2016A030306025 805296345055 201506010098 2014A020221047 2016A030313855 A1-AFD018161Z1510 A1-AFD018171Z11102 A1-AFD018171Z11101 A1-3002-16-111-003 20181132 20182044 2017 M612644 2018 T110861 2017 M622669 2017A030310213 2016kzdxm032 2017B030314166 YN2018MJ07 YN2018QJ08

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出版当年[2018]版:
大类 | 2 区 医学
小类 | 2 区 药学
最新[2025]版:
大类 | 2 区 医学
小类 | 2 区 药学
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出版当年[2017]版:
Q1 PHARMACOLOGY & PHARMACY
最新[2023]版:
Q1 PHARMACOLOGY & PHARMACY

影响因子: 最新[2023版] 最新五年平均 出版当年[2017版] 出版当年五年平均 出版前一年[2016版] 出版后一年[2018版]

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第一作者机构: [1]School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou, Guangdong, China [2]Integrative Research Laboratory of Breast Cancer, Discipline of Integrated Chinese and Western Medicine, the Research Center of Integrative Medicine, School of Basic Medical Sciences & the Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China
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通讯作者:
通讯机构: [2]Integrative Research Laboratory of Breast Cancer, Discipline of Integrated Chinese and Western Medicine, the Research Center of Integrative Medicine, School of Basic Medical Sciences & the Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China [3]Guangdong Provincial Key Laboratory of Clinical Research on Traditional Chinese Medicine Syndrome, Guangdong Provincial Academy of Chinese Medical Sciences, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, Guangdong, China [4]Post-doctoral Research Center, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China
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