Adaptation of the Golgi Apparatus in Cancer Cell Invasion and Metastasis

被引:33
|
作者
Bui, Sarah [1 ]
Mejia, Isabel [2 ]
Diaz, Begona [2 ,3 ,4 ]
Wang, Yanzhuang [5 ]
机构
[1] Univ Michigan, Dept Mol Cellular & Dev Biol, Ann Arbor, MI 48109 USA
[2] Harbor UCLA Med Ctr, Lundquist Inst Biomed Innovat, Dept Internal Med, Div Med Hematol & Oncol, Torrance, CA USA
[3] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA
[4] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA
[5] Univ Michigan, Sch Med, Dept Neurol, Ann Arbor, MI 48109 USA
来源
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY | 2021年 / 9卷
关键词
Golgi; cancer; dissemination; metastasis; oncogenic transformation; proliferation; signaling; tumorigenesis; GROWTH-FACTOR-ALPHA; GENE-EXPRESSION SIGNATURES; CASPASE-MEDIATED CLEAVAGE; TO-MESENCHYMAL TRANSITION; BREAST-CANCER; COLORECTAL-CANCER; PROTEIN-KINASE; CATHEPSIN S; O-GLYCAN; HEPATOCELLULAR-CARCINOMA;
D O I
10.3389/fcell.2021.806482
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The Golgi apparatus plays a central role in normal cell physiology by promoting cell survival, facilitating proliferation, and enabling cell-cell communication and migration. These roles are partially mediated by well-known Golgi functions, including post-translational modifications, lipid biosynthesis, intracellular trafficking, and protein secretion. In addition, accumulating evidence indicates that the Golgi plays a critical role in sensing and integrating external and internal cues to promote cellular homeostasis. Indeed, the unique structure of the mammalian Golgi can be fine-tuned to adapt different Golgi functions to specific cellular needs. This is particularly relevant in the context of cancer, where unrestrained proliferation and aberrant survival and migration increase the demands in Golgi functions, as well as the need for Golgi-dependent sensing and adaptation to intrinsic and extrinsic stressors. Here, we review and discuss current understanding of how the structure and function of the Golgi apparatus is influenced by oncogenic transformation, and how this adaptation may facilitate cancer cell invasion and metastasis.
引用
收藏
页数:20
相关论文
共 50 条
  • [1] Inhibition of cancer cell invasion and metastasis by genistein
    Pavese, Janet M.
    Farmer, Rebecca L.
    Bergan, Raymond C.
    CANCER AND METASTASIS REVIEWS, 2010, 29 (03) : 465 - 482
  • [2] The Role of Drebrin in Cancer Cell Invasion
    Dart, Anna E.
    Gordon-Weeks, Phillip R.
    DREBRIN: FROM STRUCTURE AND FUNCTION TO PHYSIOLOGICAL AND PATHOLOGICAL ROLES, 2017, 1006 : 375 - 389
  • [3] Inhibition of cancer cell invasion and metastasis by genistein
    Janet M. Pavese
    Rebecca L. Farmer
    Raymond C. Bergan
    Cancer and Metastasis Reviews, 2010, 29 : 465 - 482
  • [4] Roles of Arf6 in cancer cell invasion, metastasis and proliferation
    Li, Rui
    Peng, Cheng
    Zhang, Xianzhe
    Wu, Yuewei
    Pan, Shida
    Xiao, Yechen
    LIFE SCIENCES, 2017, 182 : 80 - 84
  • [5] Dance of The Golgi: Understanding Golgi Dynamics in Cancer Metastasis
    Bajaj, Rakhee
    Warner, Amanda N.
    Fradette, Jared F.
    Gibbons, Don L.
    CELLS, 2022, 11 (09)
  • [6] Regulator of G protein signaling 20 enhances cancer cell aggregation, migration, invasion and adhesion
    Yang, Lei
    Lee, Maggie M. K.
    Leung, Manton M. H.
    Wong, Yung H.
    CELLULAR SIGNALLING, 2016, 28 (11) : 1663 - 1672
  • [7] TMPRSS3 modulates ovarian cancer cell proliferation, invasion and metastasis
    Zhang, Dan
    Qiu, Shuang
    Wang, Qi
    Zheng, Jianhua
    ONCOLOGY REPORTS, 2016, 35 (01) : 81 - 88
  • [8] Non-Muscle Myosins in Tumor Progression, Cancer Cell Invasion, and Metastasis
    Ouderkirk, Jessica L.
    Krendel, Mira
    CYTOSKELETON, 2014, 71 (08) : 447 - 463
  • [9] RACK1 promotes prostate cancer cell proliferation, invasion and metastasis
    Shen, Fangrong
    Yan, Chunyin
    Liu, Ming
    Feng, Yahong
    Chen, Youguo
    MOLECULAR MEDICINE REPORTS, 2013, 8 (04) : 999 - 1004
  • [10] Cancer invasion and metastasis
    Wittekind, C
    Neid, M
    ONCOLOGY, 2005, 69 : 14 - 16