Abstract
Abstract Background: KAI1 C-terminal interacting tetraspanin (KITENIN) has been reported to promote tumor invasion and metastasis in various cancers. The aim of this study was to investigate the effect of KITENIN on biological behaviors in human gliomas and in mouse glioma models. Methods: KITENIN expression was examined using western blot, qRT-PCR and immunohistochemistry on human samples. KITENIN expression rate was compared in each histological grade, and survival rates were analyzed. Tumor invasiveness was investigated both in vitro and in vivo using stable cell lines after KITENIN-overexpression (GL261) and knock down (U251). Results: Expression of KITENIN tended to be stronger in high-grade gliomas than in low-grade gliomas by western blot & qRT-PCR on frozen human tumor samples and by immunohistochemistry on paraffin-embedded tissues as well. Proportions of strong KITENIN expression were 16.7%, 21.4%, 33.3%, and 56.8%, respectively, from grade I through IV (p=0.001). However, survival analysis using the Kaplan-Meier method did not reveal statistically significant difference between the high KITENIN expression group and the low expression group in terms of overall survival and progression free survival (p=0.55 and 0.807, respectively). In vitro assays revealed that genetic modulation of KITENIN was significantly related with tumor cell invasion & migration. Up-regulated KITENIN expression significantly affected the survival rate possibly due to increased invasiveness in orthotopic mouse glioma models. Conclusion: Strong KITENIN expression was more likely to be observed in high-grade gliomas and its up-regulation was associated with increased invasiveness supported by shorter survival rates in orthotopic mouse glioma models. Citation Format: Kyung-Hwa Lee, Kyung-Sub Moon, Eun-Jeong Ahn, Se-Jeong Oh, Sang-Hee Cho, Jae-Hyuk Lee, Shin Jung, Kyung Keun Kim. Role of KITENIN in malignant gliomas in relation to tumor invasiveness. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4695. doi:10.1158/1538-7445.AM2014-4695
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