华西口腔医学杂志 ›› 2021, Vol. 39 ›› Issue (2): 221-226.doi: 10.7518/hxkq.2021.02.015

• 综述 • 上一篇    下一篇

口腔癌颌骨侵犯的分子机制研究进展

刘伟(), 李春洁(), 李龙江   

  1. 口腔疾病研究国家重点实验室 国家口腔疾病临床医学研究中心 四川大学华西口腔医院头颈肿瘤外科,成都 610041
  • 收稿日期:2019-07-17 修回日期:2020-12-19 出版日期:2021-04-01 发布日期:2021-04-09
  • 通讯作者: 李春洁 E-mail:liuwei-scu@qq.com;lichunjie@scu.edu.cn
  • 作者简介:刘伟,硕士,E-mail:liuwei-scu@qq.com
  • 基金资助:
    四川省卫生和计划生育委员会科研课题(18PJ094);四川大学泸州市人民政府战略合作项目(2018CDLZ-12)

Advances in molecular mechanisms of bone invasion by oral cancer

Liu Wei(), Li Chunjie(), Li Longjiang   

  1. State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Dept. of Head and Neck Oncology, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China
  • Received:2019-07-17 Revised:2020-12-19 Online:2021-04-01 Published:2021-04-09
  • Contact: Li Chunjie E-mail:liuwei-scu@qq.com;lichunjie@scu.edu.cn
  • Supported by:
    Scientific Research Project of Sichuan Health and Family Planning Commission(18PJ094);Sichuan University Luzhou People,s Government Strategic Cooperation Project(2018CDLZ-12)

摘要:

口腔癌易于发生颌骨侵犯,影响患者预后,而这一现象的分子机制尚未完全阐明。目前研究发现,口腔癌细胞通过一系列信号分子的表达直接或者间接影响破骨细胞的形成和功能,有多条信号通路参与其调控,其中核因子κB受体活化因子配体/核因子κB受体活化因子/骨保护素信号通路的调节备受关注。本文就口腔癌颌骨侵犯的分子机制研究进展进行综述。

关键词: 口腔癌, 骨侵犯, 分子机制, 破骨细胞

Abstract:

Bone invasion by oral cancer is a common clinical problem, which affects the choice of treatment and predicts a poor prognosis. Unfortunately, the molecular mechanism of this phenomenon has not been fully elucidated. Current studies have revealed that oral cancer cells modulate the formation and function of osteoclasts through the expression of a series of signal molecules. Many signal pathways are involved in this process, of which receptor activator of nuclear factor-κB ligand/receptor activator of nuclear factor-κB/osteoprotegerin signaling pathway attracted much attention. In this review, we introduce recent progress in molecular mechanisms of bone invasion by oral cancer.

Key words: oral cancer, bone invasion, molecular mechanism, osteoclast

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