Wild pink bayberry free phenolic extract induces mitochondria-dependent apoptosis and G0/G1 cell cycle arrest through p38/MAPK and PI3K/Akt pathway in MDA-MB-231 cancer cells  

作　　者：Wen Xia Ersheng Gong Yanyun Lin Bisheng Zheng Wenhan Yang Tong Li Sheng Zhang Peng Li Ruihai Liu 

机构地区：[1]Overseas Expertise Introduction Center for Discipline Innovation of Food Nutrition and Human Health(111 Center),School of Food Science and Engineering,South China University of Technology,Guangzhou 510641,China [2]School of Public Health and Health Management,Gannan Medical University,Ganzhou 341000,China [3]Key Laboratory of Tropical Crop Products Processing of Ministry of Agriculture and Rural Affairs,Agricultural Products Processing Research Institute,Chinese Academy of Tropical Agricultural Sciences,Zhanjiang 524001,China [4]Department of Food Science,Cornell University,Ithaca 14853,USA [5]Stem Cell Research and Cellular Therapy Center,Affi liated Hospital of Guangdong Medical University,Zhanjiang 524001,China

出　　处：《Food Science and Human Wellness》2023年第5期1510-1518,共9页食品科学与人类健康（英文）

基　　金：the support from the Guangdong Basic and Applied Basic Research Foundation (2020A1515011376);the National Natural Science Foundation of China (31601397);the Innovative Leading Talents Project of Guangzhou Development Zone;Guangzhou Innovation Leading Talent Project;the 111 Project (B17018)。

摘　　要：Polyphenol-rich foods have been shown to be good for cancer prevention as powerful antioxidants. In this study, the mechanisms of wild pink bayberry free phenolic extract(WPBFE)inhibiting the proliferation and inducing apoptotic of MDA-MB-231 breast cancer cells was examined. The main phenolic acids and flavonols in WPBFE were gallic acid((18.83 ± 0.44)μg/g FW)and myricetin((1.52 ± 0.05)μg/g FW), respectively. The maximum inhibition rate of WPBFE at non-cytotoxicity dose(below 80 mg/mL)was 81%. Western blotting analysis showed that WPBFE could cause the arrest of cell cycle in G0/G1 phase by down-regulating expression levels of PCNA, CDK4, cyclin D1 and up-regulating the expression level of p21. Meanwhile, WPBFE induced apoptosis through initiating the mitochondrial death pathway by up-regulating cleaved caspase-3 and enhancing the ratio of Bax/Bcl-2, with the maximum expression levels of 1.29 and 2.03 folds that of control group, respectively. Further study of the upstream protein, we found that WPBFE down-regulated TRAF2, while upregulated p-ASK1, p-p38 and p-p53. Furthermore, WPBFE could down-regulate the expression of p-PI3K and p-Akt. These observations indicated that WPBFE might play an anticancer role through regulating the p38 MAPK together with PI3K/Akt pathway.

关 键 词：Phenolic extract Breast cancer Cell cycle Apoptosis Cell proliferation 

分 类 号：R285[医药卫生—中药学]