Expression of FAP-1 Correlates with Glioblastoma Proliferation, Migration and Treatment Resistance

Abstract Background: Glioblastoma (GBM) is the most severe type of brain cancer, with an extremely high mortality rate and the average survival time less than 15 months. Almost in all GBM cases, the residual tumor cells continue to divide uncontrollably, leading to tumor re-establishment, i.e., tumor recurrence, and ultimately death. Therefore, there is an urgent need to identify critical mediators of GBM progression and resistance to therapy. Fas-associated Phosphatase-1 (FAP-1, also known as PTPN13 or PTPL1) is a member of a large protein tyrosine phosphatase family. It has been shown that FAP-1 expression is downregulated in many types of cancers, which leads to unabated signaling and tumor progression and metastasis. The aim of this study is to evaluate the role of FAP-1 in GBM progression and resistance to therapy.Methods: Cell viability assays, radiotherapy and temozolomide response assays, and Western blot were used to analysis of FAP-1 in GBM based on Oncomine.Results: Our results showed that knockdown of FAP-1 enhanced viability and migration of GBM cell lines, and importantly, increased GBM cell resistance to radiotherapy and temozolomide. Conclusions: FAP-1 is important for GBM cells, and may account for GBM resistance to therapy.