Abstract
Tripartite motif protein 32 (TRIM32), an E3 ubiquitin ligase, has been reported to participate in many human cancers. However, the underlying role of TRIM32 in glioma remains largely unknown. Here, we aimed to explore the function of TRIM32 in glioma cells and the clinical implications and found that TRIM32 was upregulated in glioma tissues. Consistently, overexpression of TRIM32 promoted glioma U87 and U251 cell proliferation and conferred cell resistance to temozolomide (TMZ). Conversely, knockdown of TRIM32 inhibited glioma cells proliferation in vitro and in vivo and sensitized glioma cells to the treatment of TMZ in a p53-dependent and -independent manner. Mechanistically, knockdown of TRIM32 induced apoptosis of U87 an U251 cells. In addition, TRIM32 interacted with the antiapoptotic proteins BCL-xL and BCL-w, which antagonized the inhibitory effect of TRIM32 knockdown in U87 cells. Together, our study uncovered the role of TRIM32 in glioma and TRIM32 may be a potential therapeutic target for gliomas.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Biochemical and Biophysical Research Communications
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
