Abstract
C-X-C chemokine receptor 2 (CXCR2), a member of the G-protein-coupled receptor family, is an interleukin-8 receptor and results in the activation of neutrophils. To date, CXCR2 has been identified with many cell events, including inflammation, neovascularization, metastasis, and cell carcinogenesis. This study aimed to investigate alterations in the expression of CXCR2 in patients with brain gliomas and relationships with pathological grades and clinicopathological characteristics. Brain tissue specimens from 60 patients with glioma and 15 patients undergoing surgery for epilepsy (controls) were detected using streptavidin-perosidase immunohistochemistry. Western blotting was used to evaluate CXCR2 protein levels with fresh tissues derived from glioma cases or controls. Correlations between CXCR2 expression and clinicopathological characteristics were analyzed using SPSS software. The results showed high-grade gliomas with high CXCR2 expression as compared with normal tissues. The expression of CXCR2 was significantly related to high grades and recurrence of tumor but not to age or sex. During an in vitro wound healing assay, U251 migration was reduced when the CXCR2-specific inhibitor SB225002 was applied. Our results suggested that the high expression of CXCR2 in gliomas was closely correlated to the degree of malignancy and recurrence and that CXCR2 inhibition decreased the migration of glioma cells. Therefore, CXCR2 may serve as a potential therapeutic target for the recurrence and migration of gliomas.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.