APLNR stimulates the development of glioma via the NFAT5/AKT feedback loop

Z.-P. Zhang, X.-Q. Sun, S.-J. Yuan

Department of Brain Center, Sunshine Integration Hospital Shandong Chine, Weifang, China. zhao-peng-zhang@163.com

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• Oncology

OBJECTIVE: To detect the role of APLNR in influencing the proliferative ability and development of glioma.

PATIENTS AND METHODS: APLNR levels in 42 matched glioma tissues and adjacent normal brain tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between APLNR level and clinical features of glioma patients was assessed. Regulatory effects of APLNR on glioma cell functions were evaluated by cell counting kit-8 (CCK-8), colony formation, and 5-Ethynyl-2’-deoxyuridine (EdU) assay, respectively. At last, the involvement of NFAT5 in APLNR-regulated glioma cell phenotypes was examined.

RESULTS: APLNR was upregulated in glioma tissues than the adjacent ones. Glioma patients expressing higher level of APLNR had more advanced stage and worse prognosis. Knockdown of APLNR inhibited proliferative ability of glioma. NFAT5 level was negatively regulated by APLNR. Notably, NFAT5 could partially abolish the regulatory effect of APLNR on glioma cell phenotypes.

CONCLUSIONS: APLNR level is closely linked to tumor grading and prognosis of glioma patients. It stimulates proliferative ability in glioma cells by targeting NFAT5.

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