第10号染色体缺失的磷酸酶和张力蛋白同源基因在口腔鳞状细胞癌中的作用

Effect of phosphatase and tensin homolog gene deleted on chromosome 10 in oral squamous cell carcinoma

第10号染色体缺失的磷酸酶和张力蛋白同源基因(PTEN)可通过信号转导通路调控细胞周期,影响细胞的生长发育和程序性死亡,参与调节细胞的迁移和黏附,维护免疫系统的稳定。在口腔鳞状细胞癌(OSCC)的发生发展过程中,可能并不存在PTEN基因的突变和缺失,却可能与PTEN m RNA表达水平降低有一定的关系。PTEN蛋白在健康黏膜和口腔黏膜下纤维性变(OSF)到OSCC的不同组织学类型标本中表达逐渐下降,是OSF的发病机制和恶性转化机制中的重要分子事件。PTEN蛋白与OSCC的组织学和生物学行为有关,可作为其未来的预后指标。在多种肿瘤中,各种调控所导致PTEN蛋白的低表达,影响PTEN蛋白参与的多级信号转导,导致其在协调细胞周期进展,控制程序性细胞死亡及细胞黏附,抑制癌细胞转移和增殖等方面难以发挥预期的作用。

Phosphatase and tensin homolog gene deleted on chromosome 10（PTEN） plays an essential role not only in cell cycle regulation, limiting cell growth, and proliferation, but also in cell migration regulation, adhesion, and maintenance of the stability of the immune system through the signal transduction pathway. The PTEN gene may not undergo mutation and deletion during the development of oral squamous cell carcinoma（OSCC） but may be specifically related to the reduction of the PTEN mRNA expression level. The PTEN protein exhibits decreased expression in different histological types of specimens, ranging from healthy oral mucosa and oral submucous fibrosis（OSF） to OSCC. This event is important in the pathogenesis and malignant transformation mechanism of OSF. The expression of the PTEN protein is related to the histological and biological behavior of OSCC and can be used as a prognostic indicator of OSCC. The low expression of the PTEN protein caused by different factors may cause difficulty in performing its role on coordination of cell cycle, control of programmed cell death and cell adhesion, inhibition of metastasis and proliferation of cancer cells.