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作 者:Xue Liu Huichun Liang Huan Fang Ji Xiao Chuanyu Yang Zhongmei Zhou Jing Feng Ceshi Chen
机构地区:[1]Medical College,Anhui University of Science and Technology,Huainan 232001,China [2]Department of Laboratory Medicine&Central Laboratory,Fengxian District Central Hospital of Shanghai,Shanghai 201499,China [3]Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province,Kunming Institute of Zoology,Chinese Academy of Sciences,Kunming 650201,China [4]College of Life Science and Technology,Guangzhou Jinan Biomedicine Research and Development Center,Jinan University,Guangzhou 510632,China [5]The School of Continuing Education,Kunming Medical University,Kunming 650500,China [6]Academy of Biomedical Engineering,Kunming Medical University,Kunming 650500,China [7]The Third Affiliated Hospital,Kunming Medical University,Kunming 650106,China [8]The Second Affiliated Hospital of the Chinese University of Hong Kong,Shenzhen 518172,China
出 处:《Acta Biochimica et Biophysica Sinica》2023年第9期1487-1495,共9页生物化学与生物物理学报(英文版)
基 金:supported by the grants from National Key R&D Program of China(No.2020YFA0112300 to C.C.);the National Natural Science Foundation of China(Nos.82203413 to H.L.,81830087 and U2102203 to C.C.,82173044 to J.F.);the Yunnan Fundamental Research Projects(No.202101AS070050 to H.L.);the Yunnan Applied Basic Research Projects(Nos.202001AU070095 and 202201AT070290 to H.L.);the Yunnan Provincial Department of Education Science Research Fund Project(No.2019J1059 to H.L.).
摘 要:Angiopoietin-1(ANG1)is a pro-angiogenic regulator that contributes to the progression of solid tumors by stimulating the proliferation,migration and tube formation of vascular endothelial cells,as well as the renewal and stability of blood vessels.However,the functions and mechanisms of ANG1 in triple-negative breast cancer(TNBC)are unclear.The clinical sample database shows that a higher level of ANG1 in TNBC is associated with poor prognosis compared to non-TNBC.In addition,knockdown of ANG1 inhibits TNBC cell proliferation and induces cell cycle G1 phase arrest and apoptosis.Overexpression of ANG1 promotes tumor growth in nude mice.Mechanistically,ANG1 promotes TNBC by upregulating carboxypeptidase A4(CPA4)expression.Overall,the ANG1-CPA4 axis can be a therapeutic target for TNBC.
关 键 词:ANGIOPOIETIN-1 carboxypeptidase A4 cell proliferation cell cycle triple-negative breast cancer
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