PI3K/Akt signaling in osteosarcoma
作者:
Zhang, Jian;Yu, Xiao-Hua;Yan, Yi-Guo;Wang, Cheng;Wang, Wen-Jun*
期刊:
Clinica Chimica Acta,2015年444:182-192 ISSN:0009-8981
通讯作者:
Wang, Wen-Jun
作者机构:
[Wang, Wen-Jun; Zhang, Jian; Wang, Cheng; Yan, Yi-Guo] Univ South China, Affiliated Hosp 1, Dept Spine Surg, Hengyang 421001, Hunan, Peoples R China.;[Yu, Xiao-Hua] Univ South China, Life Sci Res Ctr, Hengyang 421001, Hunan, Peoples R China.
通讯机构:
[Wang, Wen-Jun] U;Univ South China, Affiliated Hosp 1, Dept Spine Surg, Hengyang 421001, Hunan, Peoples R China.
关键词:
OS;PI3K;Akt;PTEN;mTOR
摘要:
Osteosarcoma (OS) is the most common nonhematologic bone malignancy in children and adolescents. Despite the advances of adjuvant chemotherapy and significant improvement of survival, the prognosis remains generally poor. As such, the search for more effective anti-OS agents is urgent. The phosphatidylinositol 3-kinase (PI3K)/Akt pathway is thought to be one of the most important oncogenic pathways in human cancer. An increasing body of evidence has shown that this pathway is frequently hyperactivated in OS and contributes to disease initiation and development, including tumorigenesis, proliferation, invasion, cell cycle progression, inhibition of apoptosis, angiogenesis, metastasis and chemoresistance. Inhibition of this pathway through small molecule compounds represents an attractive potential therapeutic approach for OS. The aim of this review is to summarize the roles of the PI3K/Akt pathway in the development and progression of OS, and to highlight the therapeutic potential of targeting this signaling pathway. Knowledge obtained from the application of these compounds will help in further understanding the pathogenesis of OS and designing subsequent treatment strategies. © 2015 Elsevier B.V.
语种:
英文
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Foam cells in atherosclerosis
作者:
Yu, Xiao-Hua;Fu, Yu-Chang;Zhang, Da-Wei;Yin, Kai*;Tang, Chao-Ke
期刊:
Clinica Chimica Acta,2013年424:245-252 ISSN:0009-8981
通讯作者:
Yin, Kai
作者机构:
[Tang, Chao-Ke; Yu, Xiao-Hua] Univ South China, Life Sci Res Ctr, Hengyang 421001, Hunan, Peoples R China.;[Tang, Chao-Ke; Yin, Kai] Univ South China, Key Lab Atherosclerol Hunan Prov, Inst Cardiovasc Res, Hengyang 421001, Hunan, Peoples R China.;[Fu, Yu-Chang] Univ Alabama Birmingham, Dept Nutr Sci, Birmingham, AL 35294 USA.;[Zhang, Da-Wei] Univ Alberta, Dept Pediat, Edmonton, AB T6G 2S2, Canada.;[Zhang, Da-Wei] Univ Alberta, Grp Mol & Cell Biol Lipids, Edmonton, AB T6G 2S2, Canada.
通讯机构:
[Yin, Kai] U;Univ South China, Key Lab Atherosclerol Hunan Prov, Inst Cardiovasc Res, Hengyang 421001, Hunan, Peoples R China.
关键词:
Foam cells;Atherosclerosis;CD36;ACAT1;ABCA1;ABCG1
摘要:
Atherosclerosis is a chronic disease characterized by the deposition of excessive cholesterol in the arterial intima. Macrophage foam cells play a critical role in the occurrence and development of atherosclerosis. The generation of these cells is associated with imbalance of cholesterol influx, esterification and efflux. CD36 and scavenger receptor class A (SR-A) are mainly responsible for uptake of lipoprotein-derived cholesterol by macrophages. Acyl coenzyme A:cholesterol acyltransferase-1 (ACAT1) and neutral cholesteryl ester hydrolase (nCEH) regulate cholesterol esterification. ATP-binding cassette transporters A1(ABCA1), ABCG1 and scavenger receptor BI (SR-BI) play crucial roles in macrophage cholesterol export. When inflow and esterification of cholesterol increase and/or its outflow decrease, the macrophages are ultimately transformed into lipid-laden foam cells, the prototypical cells in the atherosclerotic plaque. The aim of this review is to describe what is known about the mechanisms of cholesterol uptake, esterification and release in macrophages. An increased understanding of the process of macrophage foam cell formation will help to develop novel therapeutic interventions for atherosclerosis. © 2013 The Authors.
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英文
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