14-3-3 σ: A potential biomolecule for cancer therapy

被引:21
|
作者
Huang, Yun [1 ]
Yang, Mingxiu [1 ]
Huang, Weiguo [1 ]
机构
[1] Univ South China, Canc Res Inst, Hunan Prov Key Lab Tumor Cellular & Mol Pathol 20, Hengyang Med Coll, Hengyang 421001, Hunan, Peoples R China
基金
美国国家科学基金会;
关键词
14-3-3; proteins; sigma; Cell cycle; Tumor progression; Cancer treatment; REGULATING DNA-REPAIR; CELL-CYCLE; PROSTATE-CANCER; DOWN-REGULATION; EXOENZYME-S; EPIGENETIC INACTIVATION; CISPLATIN RESISTANCE; EXPRESSION; CARCINOMA; SUPPRESSES;
D O I
10.1016/j.cca.2020.09.009
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
As more studies have focused on the function of 14-3-3 proteins, their role in tumor progression has gradually improved. In the 14-3-3 protein family, 14-3-3 sigma is the protein that is most associated with tumor occurrence and development. In some malignancies, 14-3-3 sigma acts as a tumor suppressor via p53 and tumor suppressor genes. In most tumors, 14-3-3 sigma overexpression increases resistance to chemotherapy and radiotherapy and mediates the G2-M checkpoint after DNA damage. Although 14-3-3 sigma overexpression has been closely associated with poorer prognosis in pancreatic, gastric and colorectal cancer, its role in gallbladder and nasopharyngeal cancer remains less clear. As such, the function of 14-3-3 sigma in specific cancer types needs to be further clarified. It has been hypothesized that a role may be related to its molecular chaperone function combined with various protein ligands. In this review, we examine the role of 14-3-3 sigma in tumor development and drug resistance. We discuss the potential of targeting 14-3-3 sigma regulators in cancer therapy and treatment.
引用
收藏
页码:50 / 58
页数:9
相关论文
共 50 条
  • [21] Methylation of 14-3-3σ gene and prognostic significance of 14-3-3σ expression in non-small cell lung cancer
    Raungrut, Pritsana
    Petjaroen, Pingpond
    Geater, Sarayut Lucien
    Keeratichananont, Warangkana
    Phukaoloun, Monlika
    Suwiwat, Supaporn
    Thongsuksai, Paramee
    ONCOLOGY LETTERS, 2017, 14 (05) : 5257 - 5264
  • [22] The role of epigenetic inactivation of 14-3-3σ in human cancer
    Lodygin, D
    Hermeking, H
    CELL RESEARCH, 2005, 15 (04) : 237 - 246
  • [23] Methylation and intratumoural heterogeneity of 14-3-3 σ in oral cancer
    Bhawal, Ujjal Kumar
    Tsukinoki, Keiichi
    Sasahira, Tomonori
    Sato, Fuyuki
    Mori, Yusuke
    Muto, Noriko
    Sugiyama, Masaru
    Kuniyasu, Hiroki
    ONCOLOGY REPORTS, 2007, 18 (04) : 817 - 824
  • [24] The role of epigenetic inactivation of 14-3-3σ in human cancer
    Dmitri LODYGIN
    Heiko HERMEKING
    Cell Research, 2005, (04) : 237 - 246
  • [25] The role of epigenetic inactivation of 14-3-3σ in human cancer
    Dmitri LODYGIN
    Heiko HERMEKING
    Cell Research, 2005, 15 : 237 - 246
  • [26] 14-3-3 Proteins - a focus on cancer and human disease
    Wilker, E
    Yaffe, MB
    JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2004, 37 (03) : 633 - 642
  • [27] Breast cancer cell motility is promoted by 14-3-3γ
    Hiraoka, Emiko
    Mimae, Takahiro
    Ito, Masaoki
    Kadoya, Takayuki
    Miyata, Yoshihiro
    Ito, Akihiko
    Okada, Morihito
    BREAST CANCER, 2019, 26 (05) : 581 - 593
  • [28] Loss of 14-3-3σ in prostate cancer and its precursors
    Cheng, L
    Pan, CX
    Zhang, JT
    Zhang, SB
    Kinch, MS
    Li, L
    Baldridge, LA
    Wade, C
    Hu, ZQ
    Koch, MO
    Ulbright, TM
    Eble, JN
    CLINICAL CANCER RESEARCH, 2004, 10 (09) : 3064 - 3068
  • [29] 14-3-3 α and 14-3-3 ξ contribute to immune responses in planarian Dugesia japonica
    Lu, Qingqing
    Wu, Suge
    Zhen, Hui
    Deng, Hongkuan
    Song, Qian
    Ma, Kaifu
    Cao, Zhonghong
    Pang, Qiuxiang
    Zhao, Bosheng
    GENE, 2017, 615 : 25 - 34
  • [30] 14-3-3 β, but not 14-3-3 γ, Supports Nuclear Transport of Synaptopodin 2 (Myopodin).
    Ardestani, M. Abootorabi
    Linde, N. F.
    Papadopoulos, S.
    Pfitzer, G.
    Schroeter, M.
    MOLECULAR BIOLOGY OF THE CELL, 2014, 25