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Title: KLF8 Promotes Temozolomide Resistance in Glioma Cells via β-Catenin Activation. Author: Yu G, Wu F, Wang E. Journal: Cell Physiol Biochem; 2016; 38(4):1596-604. PubMed ID: 27081861. Abstract: BACKGROUND/AIMS: The transcription factor Krüppel-like factor (KLF) 8 plays important roles in tumorigenesis and tumor metastasis. However, the relationship between KLF8 and glioma cell chemoresistance is not known. METHODS: The effects of KLF8 on glioma cell proliferation, apoptosis and chemosensitivity to temozolomide (TMZ) were analyzed by Cell Counting Kit 8 assay and flow cytometry assay. A xenograft model was used to study the effect of KLF8 on tumor growth and sensitivity to TMZ. RESULTS: We found that in the absence of KLF8, glioma cells showed greater sensitivity to TMZ, resulting in the inhibition of cell growth and enhanced apoptosis. KLF8 overexpression had the opposite effect; that is, cell resistance to TMZ was increased, which was associated with β-catenin activation. CONCLUSION: Taken together, these data suggest that KLF8 modulates glioma cell resistance to TMZ via activation of β-catenin; therefore, therapies that inhibit KLF8 levels in glioma can enhance the efficacy of TMZ treatment.[Abstract] [Full Text] [Related] [New Search]