Research on the role of HSP27 and Fas/Fasl in the invasion and metastasis of triple negative breast cancer
10.3969/j.issn.1000-8179.20141741
- VernacularTitle:HSP27与FAS/FASL在三阴性乳腺癌侵袭转移中的作用
- Author:
Kaili ZHANG
;
Hong JI
;
Ying WANG
;
Weiyuan MA
- Publication Type:Journal Article
- Keywords:
triple negative breast cancer;
HSP27;
fatty acid synthetase;
fatty acid synthetase ligand
- From:
Chinese Journal of Clinical Oncology
2015;(3):147-151
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the relationship between the expression of heat shock protein 27 (HSP27) in triple negative breast cancer (TNBC) and the clinico-pathological indexes of breast cancer, investigate the correlation between HSP27 and the fatty acid syn-thetase (FAS)/fatty acid synthetase ligand (FASL) of the cell apoptosis system in the Fas/Fasl system, and study the role of HSP27 in the invasion and metastasis of TNBC. Methods:The immunohistochemical S-P method was used to detect the expression of HSP27 and (FAS)/(FASL) in 100 TNBS tissue sampres, 100 non-TNBS tissue sampres, and 50 paraneoplastic tissues. This method was also used to analyze the correlations between the expression of HSP27 and the clinical and pathological indexes of TNBC, as well as be-tween the HSP27 expression and FAS/FASL expression. Results: HSP27 expression was significantly higher in TNBC than in the non-TNBC and paraneoplastic tissues (P<0.05). Statistically significant differences were observed in the FAS/FASL expression in the TNBC, non-TNBC, and paraneoplastic tissues (P<0.05). HSP27 expression had a negative correlation with FAS expression (P<0.05). HSP27 expression was positively correlated with FASL expression (P<0.05). FAS expression had a negative correlation with FASL ex-pression (P<0.05). HSP27 expression in TNBC was not correlated with age, staging, and tumor size (P>0.05), whereas HSP27 expres-sion was correlated with lymph node metastasis, number of nodal metastases, and P53 and Ki67 expression (P<0.05). Conclusion:The overexpression of HSP27 and the expression dysregulation of the FAS/FASL system may play a role in promoting TNBC transfer and invasion, cell proliferation, and poor prognosis.
