Integrin-linked kinase (ILK) plays a role in integrin signaling-mediated cell-extracellular matrix interactions and is involved in signal transduction pathways to control cell survival, differentiation, and proliferation in mammalian cells. ILK has been implicated in the progression of several human malignancies. However, its function in malignant tumors is not fully enunciated. Previous in vitro studies also implicated ILK in the regulation of E-cadherin expression and vascular endothelial growth factor expression. In the current study, we investigated the protein expression of ILK and its correlation with clinicopathological profiles, E-cadherin expression, microvessel density (MVD) and clinical outcome in 57 lung squamous cell carcinoma and 44 adenocarcinoma, using immunohistochemistry. No ILK was detected in normal bronchial epithelium, while it was positively expressed in 39 (68.42%) squamous cell carcinoma cases and 27 (61.36%) adenocarcinoma cases. Positive ILK expression was significantly associated with advanced TNM stage (P = 0.022) in adenocarcinoma, and associated with high MVD in lung squamous cell carcinoma (P < 0.001) and adenocarcinoma (P = 0.049). The Spearman's correlation test revealed that increased ILK expression was correlated with reduced E-cadherin expression in lung squamous cell carcinoma (correlation coefficient = 0.364, P = 0.005). Moreover, the Kaplan-Meier survival analysis showed that ILK, E-cadherin, and MVD were all statistically significant prognostic factors in patients with lung squamous cell carcinoma and adenocarcinoma. Measuring ILK and E-cadherin expression, and MVD may contribute to a better understanding of the prognosis of patients with lung squamous cell carcinoma and adenocarcinoma.
Objective: To investigate the expression of fragile histidine triad (FHIT) and p53 protein in non-small cell lung cancer (NSCLC) and explore the relationship between their expressions and the clinicopathological features. Methods: FHIT protein and p53 protein were detected by immunohistochemistry in 76 cases of NSCLCs and matched normal lung tissues. Results: Fifty-one cases (67.1%) showed negative expression of FHIT (apparent reduction or loss) and thirty-seven cases (48.7%) showed p53 positive expression (overexpression). The difference was significant (P=0.04). However, there was no significant difference in FHIT expression between the p53-positive group and the p53-negative group (64.9% versus 69.2%, P=0.686). The negative rate of FHIT protein expression was higher in squamous cell carcinoma than in adenocarcinoma, in moderately and poorly differentiated carcinoma than in well-differentiated carcinoma, and in cases with smoking history than in cases without smoking history (P<0.05). There was no relationship between FHIT expression and clinical stage or lymph node metastasis. The negative FHIT expression was not an independent predictor of overall survival (P=0.338). Conclusion: The frequency of negative expression of FHIT protein is higher than that of positive expression of p53 in NSCLCs. The negative expression of FHIT is independent of the expression of p53. The change of expression of FHIT may play a role in the smoking related lung tumorigenesis while it may have no relationship with the progress of NSCLC or prognosis of the patients.
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