Expression and prognostic significance of MAP4K4 in lung adenocarcinoma

Accumulating evidence indicates that mitogen-activated protein 4 kinase 4 (MAP4K4) is frequently overexpressed in many types of human cancers, and plays important roles in transformation, invasiveness, adhesion, and cell migration. The aim of the present study was to explore the expression and progn...

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Veröffentlicht in:Pathology, research and practice research and practice, 2012-09, Vol.208 (9), p.541-548
Hauptverfasser: Qiu, Mei-Hua, Qian, Yi-Ming, Zhao, Xiang-Li, Wang, Shou-Mei, Feng, Xiao-Jun, Chen, Xin-Fang, Zhang, Shu-Hui
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Sprache:eng
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Zusammenfassung:Accumulating evidence indicates that mitogen-activated protein 4 kinase 4 (MAP4K4) is frequently overexpressed in many types of human cancers, and plays important roles in transformation, invasiveness, adhesion, and cell migration. The aim of the present study was to explore the expression and prognostic significance of MAP4K4 in lung adenocarcinoma. The results of real-time quantitative PCR and Western blotting analysis revealed an enhanced expression of MAP4K4 in lung adenocarcinomas relative to adjacent non-tumorous lung tissues at both transcriptional and translational levels. Immunohistochemistry showed that 130 of 309 (42%) lung adenocarcinomas had high expression of MAP4K4. MAP4K4 overexpression was significantly correlated with histological grade (p=0.027), pT status (p=0.048), pN status (p=0.006), and pleural invasion (p=0.024). Patients with high MAP4K4 expression had a shorter overall survival compared with those with low MAP4K4 expression, regardless of histological grade, pT status, pN status, or pleural invasion status. Multivariate analysis identified MAP4K4 as an independent prognostic factor for lung adenocarcinoma. In conclusion, our results demonstrate that elevated MAP4K4 expression is closely associated with lung adenocarcinoma progression and has an independent prognostic value in predicting overall survival for patients with lung adenocarcinoma.
ISSN:0344-0338
1618-0631
DOI:10.1016/j.prp.2012.06.001