已发表论文

Bit1 沉默通过激活 IL-6/STAT3 信号通路增强胶质瘤细胞的增殖、迁移和侵袭

 

Authors Wang Z, Yin M, Wang R, Liu X, Yan D

Received 27 November 2019

Accepted for publication 12 February 2020

Published 24 March 2020 Volume 2020:13 Pages 2469—2481

DOI https://doi.org/10.2147/OTT.S240081

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Carlos E Vigil

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.
Keywords: glioma, anoikis, Bcl-2 inhibitor of transcription 1, IL-6/STAT3 signaling pathway




Figure 2 Expression of Bit1 in different glioma cell lines...