Prognostic Value of MACC1 and c-met Expressions in Non-small Cell Lung Cancer

Xingsheng HU, Xi FU, Shimin WEN, Xinyi ZOU, Yusong LIU

Abstract


Background and objective It has been proven that metastasis-associated in colon cancer 1 (MACC1) is a new gene that is related to the invasion and metastasis of tumors. MACC1 also regulates c-met expression. The aim of this study is to explore the expressions of MACC1 and hepatocyte growth factor receptor (c-met), and its relationship with invasion, metastasis, and prognosis of non-small cell lung cancer (NSCLC). Methods MACC1 and c-met expressions were detected in 103 cases of NSCLC and 40 cases of neighboring normal lung cancer tissue using immunohistochemistry. Results MACC1 and c-met expressions were significantly higher in lung cancer tissues than that in neighboring normal tissue (P<0.001). MACC1 and c-met expressions were associated with poor differentiation, advanced T stages, lymph node metastasis, and advanced TNM stages (P<0.05) of NSCLC, but not with sex, age, smoking, and histological classification (P>0.05). In addition, a positive correlation between MACC1 and c-met expressions was observed (r=0.403, P<0.001). The result from the Kaplan-Meier survival analysis showed that the five-year survival rate in patients with positive MACC1 and c-met expressions was remarkanly lower than that in patients with negative expressions (P<0.05). The result from the Cox regression analysis showed that MACC1 expression was an independent prognostic factor for NSCLC (P=0.026). Conclusion MACC1 and c-met have an important function in the differentiation, invasion, and metastasis of NSCLC. MACC1 and c-met have poor prognosis in patients with NSCLC. Moreover, MACC1 expression is an independent prognostic factor for NSCLC.

DOI: 10.3779/j.issn.1009-3419.2012.07.02

Keywords


Lung neoplasms; MACC1; c-met; Invasion; Metastasis; Prognosis

Full Text: PDF HTML

    

0 Citation
Alert me when cited by CSCD.
 



Creative Commons License
This work is licensed under a Creative Commons Attribution 3.0 License.