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学科主题: 临床医学
题名:
Synuclein gamma protects Akt and mTOR and renders tumor resistance to Hsp90 disruption
作者: Liang, W.1; Miao, S.1; Zhang, B.1; He, S.1; Shou, C.2; Manivel, P.3; Krishna, R.3; Chen, Y.4; Shi, Y. E.1,5
刊名: ONCOGENE
发表日期: 2015-04-30
DOI: 10.1038/onc.2014.126
卷: 34, 期:18, 页:2398-2405
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Oncology ; Cell Biology ; Genetics & Heredity
研究领域[WOS]: Biochemistry & Molecular Biology ; Oncology ; Cell Biology ; Genetics & Heredity
关键词[WOS]: BREAST-CANCER CELLS ; ENDOPLASMIC-RETICULUM STRESS ; ESTROGEN-RECEPTOR ; INDUCED APOPTOSIS ; ALPHA-SYNUCLEIN ; TYROSINE KINASE ; UP-REGULATION ; CHAPERONE ; GENE ; METASTASIS
英文摘要:

Heat shock protein (Hsp)90 regulates many key pathways in oncogenesis, including Akt and mammalian target of rapamycin (mTOR). The strengths of disruption of Hsp90 in cancer therapy include their versatility in inhibiting a wide range of oncogenic pathways. The present study demonstrated that synuclein. (SNCG) protects the functions of Akt and mTOR in the condition when the function of Hsp90 is blocked. Disruption of Hsp90 abolished Akt activity and mTOR signaling. However, expression of SNCG restored Akt activity and mTOR signaling. SNCG bound to Akt and mTOR in the presence and absence of Hsp90. Specifically, the C-terminal (Gln106-Asp127) of SNCG bound to the loop connecting alpha C helix and beta 4 sheet of the kinase domain of Akt. SNCG renders resistance to 17-AAG-induced apoptosis both in vitro and in tumor xenograft. A clinical follow-up study indicates that patients with an SNCG-positive breast cancer have a significantly shorter disease-free survival and overall survival than patients with SNCG-negative tumors. The present study indicates that SNCG protects Hsp90 client proteins of Akt and mTOR, and renders drug resistance to Hsp90 disruption.

语种: 英语
所属项目编号: 81230054 ; 91029739 ; 2013BAI01B06
项目资助者: State Key Program of National Natural Science Foundation of China ; National Key Technology R&amp ; D Program for the 12th Five-year Plan of China ; State Key Laboratory of Reproductive Medicine ; Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
WOS记录号: WOS:000353824800012
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/51870
Appears in Collections:北京大学临床肿瘤学院_期刊论文

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作者单位: 1.Nanjing Med Univ, Affiliated Hosp 1, Dept Oncol, Nanjing 210029, Jiangsu, Peoples R China
2.Peking Univ, Beijing Canc Hosp & Inst, Sch Oncol, Beijing 100871, Peoples R China
3.Pondicherry Univ, Sch Life Sci, Ctr Bioinformat, Pondicherry, India
4.Zhejiang Univ, Sch Med, Womens Hosp, Dept Surg, Hangzhou 310006, Zhejiang, Peoples R China
5.Nanjing Med Univ, State Key Lab Reprod Med, Nanjing 210029, Jiangsu, Peoples R China

Recommended Citation:
Liang, W.,Miao, S.,Zhang, B.,et al. Synuclein gamma protects Akt and mTOR and renders tumor resistance to Hsp90 disruption[J]. ONCOGENE,2015,34(18):2398-2405.
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