Abstract 62P
Background
Glioma is the most common primary tumor of the human central nervous system. It is characterized by fast growth, strong invasion and impossible to complete surgical resection. Despite advances in tumor diagnosis and treatment, including surgery, radiotherapy and chemotherapy, the median survival for WHO Grade II gliomas is 5 years, for WHO Grade III gliomas is 2-3 years, and for WHO Grade IV gliomas is 14.6 months. The study of glioma cell formation mechanism is of great significance for the treatment of glioma. S100A12 expression was found to be highly correlated with glioma progression. Hax-1 protein has a variety of biological functions, such as anti-apoptosis, regulation of cell migration and endocytosis, and participates in invasion, metastasis and tumorigenesis in different types of tumors. However, there are few studies on the regulatory mechanisms of S100A12 and HAX-1 in glioma cells, and their mechanisms of action have not been fully analyzed.
Methods
To explore the effect and mechanism of S100A12 and HAX-1 genes on proliferation, invasion and migration of glioma cells and Lay the foundation for the study of glioma treatment. In this study, we carried out immunohistochemical investigation of S100A12 and HAX-1 in 81 glioma tissues to determine their expressions in glioma cells, and evaluate the clinical significance of S100A12 and HAX-1 in glioma patients. Futher we knockdown the S100A12 and HAX-1 by shRNA, and evaluated cell proliferation, cell migration and cell apoptosis by MTT, colony formation assay, transwell assay, flow cytometry assay and western blot.
Results
We found that S100A12 and HAX-1 were upregulated in tissues of glioma patients and the expressions were correlated to WHO stage. Further, we found that knockdown S100A12 inhibits the proliferation, migration and invasion of glioma cells through regulating cell apoptosis and EMT.
Conclusions
Both S100A12 and HAX-1 play vital roles in glioma progression, and may be important regulatory molecules for biological behaviors of glioma cell lines.
Legal entity responsible for the study
Southern University of Science and Technology Hospital.
Funding
Has not received any funding.
Disclosure
The author has declared no conflicts of interest.