FABP4 accelerates glioblastoma cell growth and metastasis through Wnt10b signalling.

Abstract

Glioblastomas are one of the most dangerous types of malignancies because of their metastatic capacity and challenge to treat with chemotherapy or radiotherapy. Hence, detailed research to explain the molecular mechanisms of glioblastoma metastasis is crucial to improve glioblastoma treatment. The expression level of fatty acid-binding protein 4 (FABP4) in glioblastoma cell lines and tissues was detected by Western blotting and quantitative Real-time polymerase chain reaction (qRT-PCR) assays. Proliferation assay, colon formation analysis and transwell/migration assay were performed to detect the relationship between FABP4 and malignant behaviors of glioblastoma cells in vitro. Subcutaneous xenograft and intravenous metastasis models were used to determine the role of FABP4 in vitro. Rescue assays were conducted to confirm the contribution of Wingless-Type MMTV Integration Site Family, Member 10B (Wnt10b) to the progression of glioblastoma cells regulated by FABP4. Glioblastoma cells exhibited a higher level of FABP4 expression than control cells, and down-regulation of FABP4 suppressed tumor cell growth and metastasis in vitro and in vivo. Wnt10b, as a regulator gene of FABP4, restored the effects of FABP4 down-regulation in glioblastoma cells. We provided substantive evidence that FABP4 is a growth and metastasis promoter in vivo and revealed that it functions in part through Wnt10b, which suggests that FABP4 might act as a probable target to block glioblastoma metastasis.