國家衛生研究院 NHRI:Item 3990099045/12228
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12145/12927 (94%)
造访人次 : 856908      在线人数 : 957
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 查询小技巧：
  • 您可在西文检索词汇前后加上"双引号"，以获取较精准的检索结果
  • 若欲以作者姓名搜寻，建议至进阶搜寻限定作者字段，可获得较完整数据
    •  进阶搜寻
    主页 ‧ 登入 ‧ 上传 ‧ 说明 ‧ 关于NHRI ‧ 管理 到手机版


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/12228


    题名: ACTL6A is a novel oncogene and prognostic biomarker for prostate cancer
    作者: Chuu, CP;Lin, CY;Huang, SH;Tsai, KKC
    贡献者: Institute of Cellular and Systems Medicine
    摘要: ACTL6A (Actin-like 6A protein) is a member of ATP-dependent SWI/SNF-like BAF chromatin remodeling complexes encoding a family of actin-related proteins. Using 3D culture and Micro-Western Array analysis targeting for epigenetic regulatory proteins, we discovered that ACTL6A plays essential role in regulation of the prostate acinar morphogenesis, a differentiation procedure. Expression level of ACTL6A protein decreases dramatically during prostate acinar morphogenesis, suggesting that ACTL6A is a potential oncogene in prostate cancer (PCa). We analyzed Oncomine online database and found that ACTL6A is higher in prostate cancer vs. adjacent normal prostate tissues, while ACTL6A protein level is even higher in metastatic PCa. High ACTL6A gene expression level in prostate tumors correlates to worse PCa patient survival outcome. We knocked down ACTL6A in PC-3 PCa cells, and the reduction of ACTL6A suppressed proliferation, migration, and invasion of PC-3 cells. Knockdown of ACTL6A also reduced population of CD44+ and ALDH enzyme activity-positive PCa cells, which represents the population of cancer stem cell (CSC) in PCa. Decrease of ACTL6A reduced expression of a few oncogenic long non-coding RNA, including HIFCAR, MALAT1, and PCAT-1. Seahorse mito-stress and glycol-stress analysis revealed that knockdown of ACTL6A suppressed OCR and ECAR of mitochondria in PCa cells. ACTL6A knockdown up-regulates expression of glycolysis-related genes, suggesting that ACTL6A regulate cancer metabolism. Our study suggested that ACTL6A regulates expression and activity of YAP and c-Myc, which in turn regulates stemness factors Nanog and Sox2, thus enhances the cancer stemness of PCa cells. ACTL6A also regulates mitochondrial function and metabolic genes PKM2, LDHA, GLS1, partially through c-Myc, therefore ACTL6A causes metabolism rewiring in PCa. All these regulations contribute to the metastasis of PCa. In conclusion, ACTL6A is a novel oncogene and prognostic biomarker for PCa.
    日期: 2019-10
    關聯: Annals of Oncology. 2019 Oct;30(Suppl. 6):Abstract number MO2-10-6.
    Link to: http://dx.doi.org/10.1093/annonc/mdz338.069
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0923-7534&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000491239300136
    显示于类别:[褚志斌] 會議論文/會議摘要

    文件中的档案:

    档案 描述 大小格式浏览次数
    ISI000491239300136.pdf75KbAdobe PDF240检视/开启


    在NHRI中所有的数据项都受到原著作权保护.

    TAIR相关文章

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回馈