基础医学与临床 ›› 2022, Vol. 42 ›› Issue (1): 159-162.doi: 10.16352/j.issn.1001-6325.2022.01.025

• 短篇综述 • 上一篇    下一篇

IL-6/JAK/STAT3信号通路在前列腺癌发展和治疗中的研究进展

陈号1, 陈韬2, 吴静1*   

  1. 1.昆明医科大学 生物化学与分子生物学系,云南 昆明 650500;
    2.昆明医科大学第二附属医院泌尿外科,云南 昆明 650101
  • 收稿日期:2021-04-15 修回日期:2021-08-13 出版日期:2022-01-05 发布日期:2022-01-05
  • 通讯作者: * wujingkm176@126.com
  • 基金资助:
    云南省科技厅-昆明医科大学应用基础研究联合专项资金[2018FE001(-237)]

Research progress on IL-6/JAK/STAT3 in the development and treatment of prostate cancer

CHEN Hao1, CHEN Tao2, WU Jing1*   

  1. 1. Department of Biochemistry and Molecular Biology, Kunming Medical University, Kunming 650500;
    2. Department of Urology, the Second Affiliated Hospital of Kunming Medical University, Kunming 650101, China
  • Received:2021-04-15 Revised:2021-08-13 Online:2022-01-05 Published:2022-01-05
  • Contact: * wujingkm176@126.com

摘要: IL-6/JAK/STAT3是IL-6激活的显著的信号通路之一。IL-6、p-STAT3在前列腺癌(PCa)组织和转移瘤中高表达,在诱导PCa发生、促进肿瘤细胞增殖、侵袭和转移中起着关键作用,并且通过激活雄激素受体(AR)参与PCa去势抵抗和肿瘤耐药。 IL-6/JAK/STAT3及其激活的下游因子在肿瘤进展中的多种角色为化疗药物开发提供了良好的基础,目前,许多靶向抑制剂已被证明可有效抑制肿瘤进展,有望研发出更多有效药物。

关键词: 前列腺癌, 去势抵抗性前列腺癌, 白细胞介素-6, 信号传导与转录激活因子3(STAT3)

Abstract: IL-6/JAK/STAT3 is one of the most significant signaling pathways activated by IL-6.IL-6 and p-STAT3 which are highly expressed in prostate cancer (PCa) tissue and metastatic tumors So this pathway may play a role in the occurrence of prostate cancer, promotion of malignant cell proliferation, invasion and metastasis of the tumor. It may also function in the development of castration resistance and drug resistance through activation androgen receptor(AR). The multiple roles of IL-6/JAK/STAT3 and its activated downstream factors in tumor progression provide a good basis for the development of chemotherapy drugs. Currently, many targeted inhibitors have been proved to be effective in inhibiting tumor progression and more effective drugs are expected to be developed.

Key words: prostate cancer, castration-resistant prostate cancer, interleukin-6, signal transducer and activator of transcription (STAT3)

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