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Bit1 Silencing Enhances the Proliferation, Migration, and Invasion of Glioma Cells Through Activation of the IL-6/STAT3 Pathway
BACKGROUND: Several studies have indicated that the anoikis effector Bcl-2 inhibitor of transcription 1 (Bit1) can promote or inhibit tumor progression depending on the nature of the malignancy. However, its regulatory effects on gliomas are unknown. METHODS: This study aimed at assessing Bit1 expre...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102891/ https://www.ncbi.nlm.nih.gov/pubmed/32273719 http://dx.doi.org/10.2147/OTT.S240081 |
Sumario: | BACKGROUND: Several studies have indicated that the anoikis effector Bcl-2 inhibitor of transcription 1 (Bit1) can promote or inhibit tumor progression depending on the nature of the malignancy. However, its regulatory effects on gliomas are unknown. METHODS: This study aimed at assessing Bit1 expression in glioma tissues and cells, its subsequent effects on glioma cell apoptosis, proliferation, invasion, and migration, and the underlying molecular mechanisms. RESULTS: The findings showed that lower Bit1 expressions in glioma tissues as well as a negative correlation between Bit1 expression and glioma grade. Additional findings also revealed that Bit1 silencing significantly inhibited anoikis and enhanced glioma cell proliferation, invasion, and migration. Further analysis showed that the decrease in Bit1 expressions led to malignancy proliferation and anoikis resistance through activation of the IL-6/STAT3 signaling pathway. CONCLUSION: Our data suggested that Bit1 may play an anti-oncogenic role in glioma cells and that a decrease in its expressions might induce glioma cell proliferation, migration, and invasion through the IL-6/STAT3 signaling pathway. |
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