High expression of TRPM8 predicts poor prognosis in patients with osteosarcoma

被引:19
|
作者
Zhao, Wei [1 ]
Xu, Huimian [1 ]
机构
[1] China Med Univ, Hosp 1, Dept Surg Oncol, 155 Nanjingbei St, Shenyang 110001, Liaoning, Peoples R China
关键词
TRPM8; osteosarcoma; prognosis; overall survival; disease-free survival; PROSTATE-CANCER CELLS; BREAST-CANCER; COLON-CANCER; CHANNELS; PROLIFERATION; INVOLVEMENT; BLADDER;
D O I
10.3892/ol.2016.4764
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The transient receptor potential melastatin member 8 (TRPM8) is a newly characterized oncoprotein involved in various malignant tumors. However, its expression pattern and biological function in osteosarcoma remain unclear. The present study aimed to explore the expression and prognostic significance of TRPM8 in osteosarcoma (OS). The results revealed that the expression of TRPM8 mRNA and protein in OS tissue was significantly higher than that in paired normal bone tissue (P<0.05). Additionally, the level of TRPM8 mRNA and protein in patients with a higher clinical stage and with distant metastasis was markedly higher than in those with a lower clinical stage and no metastasis (P<0.05). Furthermore, a high TRPM8 level was closely associated with clinical stage and distant metastasis (P=0.007 and 0.030), but not associated with the patient age (P=0.481), gender (P=0.905), tumor size (P=0.429), histological subtype (P=0.207) or anatomical location (P=0.369). In addition, OS patients with high TRPM8 expression had significantly shorter overall survival (P=0.008) and disease-free survival times (P=0.008) when compared with patients with low expression of TRPM8. In Cox multivariate analysis, TRPM8 overexpression was identified to be an independent and significant prognostic factor for overall survival (P=0.040), but not for disease-free survival (P=0.051). Collectively, the present data suggest that TRPM8 may play a crucial role in the development and progression of OS, and thus may be considered as a novel molecular target for therapy in patients with OS.
引用
收藏
页码:1373 / 1379
页数:7
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