Structure and function of FUS gene in prostate cancer

被引:13
|
作者
Ghanbarpanah, E. [1 ,2 ]
Kohanpour, M. A. [1 ,3 ]
Hosseini-Beheshti, F. [1 ,4 ]
Yari, L. [1 ,5 ]
Keshvari, M. [1 ]
机构
[1] Isfahan Univ Med Sci, Cardiovasc Res Inst, Isfahan Cardiovasc Res Ctr, Esfahan, Iran
[2] Islamic Azad Univ, Arsanjan Branch, Dept Biol, Arsanjan, Iran
[3] Islamic Azad Univ, Lamerd Branch, Dept Phys Educ, Lamerd, Iran
[4] Isfahan Univ Med Sci, Med Genet Ctr Genome, Esfahan, Iran
[5] NIGEB Natl Inst Genet Engn & Biotechnol, Tehran, Iran
关键词
prostate cancer; FUS; androgen receptor; cyclin D1; ANDROGEN RECEPTOR; PROLIFERATION; MUTATIONS; TLS; IDENTIFICATION; PROGRESSION; ACTIVATION; EXPRESSION; CYCLINS; INHIBIT;
D O I
10.4149/BLL_2018_118
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND: FUS reduces the proliferator factors such as cyclin D1 and Cdk6, and increases Cdk and p27. Therefore, FUS prevents the growth of prostate cancer cells. METHODS: This review tried to summarize data about FUS gene expression in correlation with the degree of prostate cancer. To find the relevant studies, the search in PubMed, Science Direct, and Scopus were performed. RESULTS: Increasing the expression of FUS decreases and increases the rate of apoptosis of prostate cancer cells, respectively. In fact, FUS reduces the proliferator factors such as: cyclin D1 and Cdk6, and increases Cdk (an anti-proliferation factor) and p27 (a proliferative inhibitory factor). Therefore, FUS prevents the growth of prostate cancer cells. An immuno-histochemical analysis showed that FUS gene expression had an inverse correlation with the degree of prostate cancer, which suggests that patients with higher levels of FUS are more likely to survive and less likely to have bone pain. CONCLUSION: The key to FUS is the signaling of the androgen receptor and the progression of the cell cycle in prostate cancer. Based on these findings, we might be able to consider exogenous expression of FUS as a treatment for prostate cancer.
引用
收藏
页码:660 / 663
页数:4
相关论文
共 50 条
  • [21] GENE FUSIONS IN PROSTATE CANCER
    Rittenhouse, H.
    ANTICANCER RESEARCH, 2008, 28 (6B) : 4055 - 4055
  • [22] Gene therapy for prostate cancer
    J Naitoh
    A Belldegrun
    Prostate Cancer and Prostatic Diseases, 1998, 1 : 189 - 196
  • [23] Gene therapy for prostate cancer
    Sikora, K
    Pandha, H
    BRITISH JOURNAL OF UROLOGY, 1997, 79 : 64 - 68
  • [24] Gene therapy for prostate cancer
    Hrouda, D
    Dalgleish, AG
    GENE THERAPY, 1996, 3 (10) : 845 - 852
  • [25] Prostate cancer gene therapy
    Russell, PJ
    Martiniello-Wilks, R
    Lockett, LJ
    Brookes, DE
    Zandvliet, D
    Watt, F
    Molloy, PL
    Khatri, A
    Both, GW
    AUSTRALASIAN BIOTECHNOLOGY, 1998, 8 (02) : 99 - 106
  • [26] Gene therapy for prostate cancer
    Naitoh, J
    Belldegrun, A
    PROSTATE CANCER AND PROSTATIC DISEASES, 1998, 1 (04) : 189 - 196
  • [27] Gene therapy for prostate cancer
    Bower, M
    Waxman, J
    SEMINARS IN CANCER BIOLOGY, 1997, 8 (01) : 3 - 9
  • [28] Gene therapy for prostate cancer
    不详
    EUROPEAN JOURNAL OF CANCER CARE, 2001, 10 (04) : 232 - 232
  • [29] Prostate cancer gene therapy
    Ferrer, FA
    Rodriguez, R
    HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA, 2001, 15 (03) : 497 - +
  • [30] Gene therapy for prostate cancer
    Mazhar, D
    Waxman, J
    BJU INTERNATIONAL, 2004, 93 (04) : 465 - 469