Its physiological roles include ion homeostasis modulation, cell volume regulation, transepithelial transport, and regulation of electrical excitability [20]. Accumulating number of studies have reported that CLIC1 is up-regulated in many tumor cells, such as hepatocellular carcinoma [10], gallbladder carcinoma [11], gastric cancer

[12], colon cancer [13], nasopharyngeal carcinoma [21], and breast cancer [22], and plays important roles in check details tumor progression by modifying cell cycle, apoptosis, cell adhesion, and promoting tumor metastasis. For example, Chen et al. [12] found that the high levels of CLIC1 expression in gastric cancer significantly correlated with lymph node metastasis, lymphatic vessels and surrounding tissues infiltration,

pathological staging, and survival time of patients; Wang et al. [23] shown that CLIC1 expression in lung adenocarcinoma was positively correlated with the T staging of the tumor and was negatively correlated with the shorter postoperative survival time of patients; Similarly, overexpression of CLIC1 was detected in gallbladder carcinoma and also found to significantly increase Epacadostat clinical trial cell motility and invasion of the poorly metastatic gallbladder carcinoma cell line [11]. These results strongly imply that CLIC1 plays an important role in tumor advancement. However, its connection with human glioma has remained unknown. Our current study provided the evidence in support of such a connection using a cohort of 128 archived clinical glioma specimens. We first detected high expression of CLIC1 in glioma tissues compared with non-neoplastic brain tissues. Further support for a possible role of CLIC1 in glioma pathogenesis derived from the analysis that revealed a strong correlation of CLIC1 expression with the histopathological staging and inversely, with the survival of the disease. These findings are consistent with the previous reports which indicated that overexpression of CLIC1 is a potential prognostic

marker for hepatocellular carcinoma [9], gallbladder carcinoma [10], gastric cancer [11], and lung adenocarcinoma [23]. In summary, our data provide the first evidence that CLIC1 expression C-X-C chemokine receptor type 7 (CXCR-7) might play an important role in the regulation of aggressiveness in human gliomas. The elevated expression of CLIC1 might represent a valuable prognostic marker for this disease. This study adds to the current realization on the involvement of CLIC1 in tumorigenesis and progression of human malignant tumors. Acknowledgements This work was funded by National Natural Science Foundation of China (NO. 81101736, NO.81272419), Talents Supported Plan Foundation of Tangdu Hospital for Yanyang Tu (2011). References 1. Dunbar E, Yachnis AT: Glioma diagnosis: immunohistochemistry and beyond. Adv Anat Pathol 2010, 17:187–201.PubMedCrossRef 2. Deangelis LM: Brain tumors. N Engl J Med 2001, 344:114–123.PubMedCrossRef 3.