KLF8 Promotes Temozolomide Resistance in Glioma Cells via β-Catenin Activation
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 chemosensit...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
Cell Physiol Biochem Press GmbH & Co KG
2016-04-01
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| Series: | Cellular Physiology and Biochemistry |
| Subjects: | |
| Online Access: | http://www.karger.com/Article/FullText/443100 |
| Summary: | 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. |
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| ISSN: | 1015-8987 1421-9778 |