Clinical roles of autophagy-related proteins Beclin-1 and mTOR in smoking and non-smoking patients with oral leukoplakia

被引:2
|
作者
Zhang, Ping [1 ]
Zhou, Peng [2 ]
Yao, Min [3 ]
机构
[1] Fudan Univ, Natl Childrens Med Ctr, Dept Stomatol, Childrens Hosp, Shanghai 201102, Peoples R China
[2] Tongling Peoples Hosp, Dept Stomatol, Tongling 244002, Anhui, Peoples R China
[3] Nanjing Med Univ, Dept Stomatol, Affiliated Childrens Hosp, Nanjing 210003, Jiangsu, Peoples R China
关键词
Smoking; oral leukoplakia; autophagy; Beclin-1; mammalian target of rapamycin; EXPRESSION;
D O I
10.4314/ahs.v23i2.71
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: To study the expressions of autophagy-related proteins Beclin-1 and mammalian target of rapamycin (mTOR) in smoking and non-smoking patients with oral leukoplakia (OLK).Methods: A total of 240 patients diagnosed as OLK from January 2017 to December 2017 were enrolled. Beclin-1 and mTOR expressions were detected by immunohistochemistry. Their clinical data were collected. The correlations of smoking with Be-clin-1 and mTOR expressions as well as clinical factors were explored by Spearman's analysis.Results: There were significant differences in gender ratio, age, lesion location, severity and malignancy between smoking and non-smoking OLK patients (P<0.05). The positive expression rate of Beclin-1 in OLK patients with simple hyperplasia and abnormal hyperplasia in the smoking group was significantly lower than that of the non-smoking group (P<0.05). In the abnor- mal hyperplasia group, the number of cigarettes daily was significantly positively correlated with mTOR expression (r=0.843, P=0.042). After the simple hyperplasia group was included, there was a positive correlation between smoking age and positive expression rate of mTOR (r=0.942, P=0.012). For number of cigarettes and smoking age, the positive expression rates of Be-clin-1 and mTOR showed significant negative correlations (r=-0.952, P=0.003, r=-0.953, P=0.002).Conclusion: Autophagy-related proteins Beclin-1 and mTOR may be involved in the smoking-induced pathogenesis of OLK.
引用
收藏
页码:616 / 622
页数:7
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