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FOXK1基因的生物特性及其在肿瘤中的研究进展

李燕 陈瑜 何美芝 卞小慧 涂令境 崔春晖 谢朗

李燕, 陈瑜, 何美芝, 卞小慧, 涂令境, 崔春晖, 谢朗. FOXK1基因的生物特性及其在肿瘤中的研究进展[J]. 分子影像学杂志, 2019, 42(4): 518-523. doi: 10.12122/j.issn.1674-4500.2019.04.23
引用本文: 李燕, 陈瑜, 何美芝, 卞小慧, 涂令境, 崔春晖, 谢朗. FOXK1基因的生物特性及其在肿瘤中的研究进展[J]. 分子影像学杂志, 2019, 42(4): 518-523. doi: 10.12122/j.issn.1674-4500.2019.04.23
Yan LI, Yu CHEN, Meizhi HE, Xiaohui BIAN, Lingjing TU, Chunhui CUI, Lang XIE. Biological characteristics of FOXK1 and its research progress in various tumors[J]. Journal of Molecular Imaging, 2019, 42(4): 518-523. doi: 10.12122/j.issn.1674-4500.2019.04.23
Citation: Yan LI, Yu CHEN, Meizhi HE, Xiaohui BIAN, Lingjing TU, Chunhui CUI, Lang XIE. Biological characteristics of FOXK1 and its research progress in various tumors[J]. Journal of Molecular Imaging, 2019, 42(4): 518-523. doi: 10.12122/j.issn.1674-4500.2019.04.23

FOXK1基因的生物特性及其在肿瘤中的研究进展

doi: 10.12122/j.issn.1674-4500.2019.04.23
基金项目: 广东省科技计划基金(2017ZC0103);国家自然科学基金(81600444);大学生创新创业训练计划项目(201712121157)
详细信息
    作者简介:

    李燕:李 燕,本科,E-mail:liyan185581@163.com

    陈 瑜,本科,E-mail:1064097476@qq.com。李燕与陈瑜共同为第一作者

    通讯作者:

    崔春晖,博士,副主任医师,E-mail:87075472@qq.com

    谢  朗,博士,主治医师,E-mail:langxiezj@hotmail.com。崔春晖、谢 朗共同为通信作者

Biological characteristics of FOXK1 and its research progress in various tumors

  • 摘要: 叉头框K1(FOXK1)是近年来广受研究关注的FOX转录因子家族成员之一。越来越多的研究表明,FOXK1与生殖、神经和消化等多种系统的肿瘤密切相关,FOXK1可通过调节细胞周期、细胞自噬以及介导信号转导通路,参与各个系统肿瘤的发生发展,影响肿瘤侵袭、转移及患者的预后。FOXK1在各个系统肿瘤组织中的特异性表达及其作用机制的研究,为肿瘤的诊治提供了新方向。本文就FOXK1的基因特征、生物学功能及其与各系统肿瘤的关系进行综述并作展望。

     

  • 图  1  人源性FOXK1基因的染色体定位

    图  2  FOXK1的蛋白结构

    图  3  FOXK1基因在人体各组织中的表达

    图  4  FOXK1基因的亚细胞定位

    表  1  FOXK1在各种肿瘤中的表达及可能机制

    肿瘤类型FOXK1表达水平可能的调节机制参考文献
    食管癌上调尚未阐明[25]
    卵巢癌上调抑制p21转录促进细胞增殖[16]
    弥漫大B细胞淋巴瘤上调靶向miR-17[18]
    乳腺癌下调抑制Twist和VEGF转录[24]
    前列腺癌上调正向调控Wnt/β-catenin通路[19]
    神经胶质瘤上调激活Wnt/β-catenin通路[20]
    下调ZRANB2-SNHG20-FOXK1通路[21]
    胶质母细胞瘤上调激活Snail转录促进EMT[23]
    肺癌上调circMAN2B2/miR-1275/FOXK1通路[17]
    肝细胞性肝癌上调TGF-β- FOXK1 - Wnt信号通路[26]
    通过Akt/mTOR通路抑制糖酵解[27]
    胃癌上调c-jun-FOXK1通路[28]
    miR-646通过下调FOXK1抑制Bcl-2/Akt通路[24]
    LINC02163-miR-593-3p/FOXK1通路[29]
    与波形蛋白相互作用促进EMT[30]
    结直肠癌上调FOXK1- RUFY3通路[35, 36]
    与FHL2共表达诱导EMT[33]
    FOXK1-Cyr61-Snail通路[37]
    LINC01503/miR-4492/FOXK1通路[38]
    下载: 导出CSV
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出版历程
  • 收稿日期:  2019-08-20
  • 刊出日期:  2019-12-01

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