Correlation between the expression of Id-1 and hyperthermia-associated molecules in oral squamous cell carcinoma

口腔鳞状细胞癌中Id-1表达与热疗相关分子的相关性

阅读:11
作者:Jun Zhao, Shengzhi Wang, Na Liu, Xiufa Tang

Conclusions

This study revealed that there was a positive correlation between Id-1 expression and the expression of p-Akt, p-GSK3β and p-HSF1. The inhibition of Id-1 expression can improve the efficacy of hyperthermia in OSCC.

Methods

Id-1, phosphorylated protein kinase B (p-Akt), phosphorylated glycogen synthase kinase 3β (p-GSK3β) and phosphorylated heat shock factor 1 (p-HSF1) expression were assessed immunohistochemically in 76 OSCC.

Objective

To investigate the expression of inhibitor of differentiation/DNA binding (Id-1), phosphatidylinositol-3-kinase/protein kinase B pathway proteins and hyperthermia-associated protein and their association with various clinicopathological factors in oral squamous cell cancer (OSCC), and explore the relationship among them in OSCC.

Results

Id-1 (73.8%), p-Akt (65.8%), p-GSK3β (60.5%) and p-HSF1 (75%) were found to be overexpressed in most of the oral cancer samples tested, and the expressions of them are correlated with advanced clinical stage, metastasis and recurrence (p<0.01), but there is no apparent relationship with gender, age, differentiation and habits (p>0.05). Survival curves show that the survival of patients with high Id-1, p-Akt, p-GSK3β and p-HSF1 expression was significantly worse than those with low Id-1, p-Akt, p-GSK3β and p-HSF1 expression (p=0.000). Id-1 expression was significantly higher in cases with high expression of p-Akt, p-GSK3β and p-HSF1 than in those with low expression (p=0.002, p=0.003, p=0.001). Conclusions: This study revealed that there was a positive correlation between Id-1 expression and the expression of p-Akt, p-GSK3β and p-HSF1. The inhibition of Id-1 expression can improve the efficacy of hyperthermia in OSCC.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。