Neoalbaconol inhibits angiogenesis and tumor growth by suppressing EGFR-mediated VEGF production
Yu, Xinfang1,2,3,4; Li, Wei1,2,5; Deng, Qipan1,2; You, Shuo6; Liu, Haidan6; Peng, Songling1,2; Liu, Xiaolan1,2; Lu, Jingchen1,2; Luo, Xiangjian1,2; Yang, Lifang1,2; Tang, Min1,2; Weng, Xinxian1,2; Yi, Wei1,2; Liu, Wenbin3,4; Wu, Shengqi3,4; Ding, Zhihui7; Feng, Tao7; Zhou, Jian8; Fan, Jia8; Bode, Ann M.9; Dong, Zigang9; Liu, Jikai7; Cao, Ya1,2
2017-05-01
Source PublicationMOLECULAR CARCINOGENESIS
Volume56Issue:5Pages:1414-1426
AbstractNeoalbaconol, derived from Albatrellus confluens, shows anti-cancer activities in the previously study, but its role in angiogenesis is unknown. Here, we determined whether neoalbaconol could attenuate angiogenesis and how does it occur. Data demonstrated that neoalbaconol could inhibit the proliferation of breast cancer cells and induce apoptosis. Also, neoalbaconol suppressed vascular endothelial growth factor (VEGF)-induced human umbilical vascular endothelial cells (HUVECs) proliferation, migration, invasion, and capillary-like tube formation in vitro and reduced tumor angiogenesis in vivo. VEGF receptor activation and the downstream signal transduction cascades activation were inhibited by neoalbaconol. Additionally, neoalbaconol blocked EGFR-mediated VEGF production. EGFR overexpression reversed the neoalbaconol-induced VEGF reduction, confirming the importance of the EGFR inhibition in anti-angiogenesis of neoalbaconol. Furthermore, neoalbaconol inhibited tumor growth and tumor angiogenesis in a breast cancer xenograft model in vivo. Taken together, these results indicate that neoalbaconol could inhibit tumor angiogenesis and growth through direct suppression effects on vascular endothelial cells and reduction of proangiogenic factors in cancer cells.
KeywordAngiogenesis Breast Cancer Egfr Neoalbaconol Vegf
DOI10.1002/mc.22602
Indexed BySCI
Language英语
WOS IDWOS:000399592100004
Citation statistics
Document Type期刊论文
Identifierhttp://ir.kib.ac.cn/handle/151853/51192
Collection植物化学与西部植物资源持续利用国家重点实验室
Affiliation1.Cent S Univ, Key Lab Canc Carcinogenesis & Invas, Chinese Minist Educ, Xiangya Hosp, Changsha, Hunan, Peoples R China
2.Cent S Univ, Xiangya Sch Med, Canc Res Inst, 110 Xiang Ya Rd, Changsha, Hunan, Peoples R China
3.Cent S Univ, Xiangya Sch Med, Hunan Canc Hosp, Changsha, Hunan, Peoples R China
4.Cent S Univ, Xiangya Sch Med, Affiliated Canc Hosp, Changsha, Hunan, Peoples R China
5.Cent S Univ, Xiangya Hosp 3, Dept Radiol, Changsha, Hunan, Peoples R China
6.Cent S Univ, Xiangya Hosp 2, Changsha, Hunan, Peoples R China
7.Chinese Acad Sci, Kunming Inst Bot, State Key Lab Phytochem & Plant Resources West Ch, Kunming, Yunnan, Peoples R China
8.Zhongshan Hosp, Liver Canc Inst, Chinese Minist Publ Hlth, Key Lab Carcinogenesis, Shanghai, Peoples R China
9.Univ Minnesota, Hormel Inst, 801 16th Ave NE, Austin, MN 55912 USA
Recommended Citation
GB/T 7714
Yu, Xinfang,Li, Wei,Deng, Qipan,et al. Neoalbaconol inhibits angiogenesis and tumor growth by suppressing EGFR-mediated VEGF production[J]. MOLECULAR CARCINOGENESIS,2017,56(5):1414-1426.
APA Yu, Xinfang.,Li, Wei.,Deng, Qipan.,You, Shuo.,Liu, Haidan.,...&Cao, Ya.(2017).Neoalbaconol inhibits angiogenesis and tumor growth by suppressing EGFR-mediated VEGF production.MOLECULAR CARCINOGENESIS,56(5),1414-1426.
MLA Yu, Xinfang,et al."Neoalbaconol inhibits angiogenesis and tumor growth by suppressing EGFR-mediated VEGF production".MOLECULAR CARCINOGENESIS 56.5(2017):1414-1426.
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