Journal
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
Volume 36, Issue -, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/s13046-017-0606-1
Keywords
Glioma; Proliferation; YAP; beta-catenin; GSK3 beta; Nude mice
Categories
Funding
- National Natural Science Foundation of China [81372699, 81472345, 81672489]
- 333 talent project of Jiangsu Province [BRA2015394]
- Six major talent summit of Jiangsu Province [WSW-039]
Ask authors/readers for more resources
Background: Hippo/YAP pathway is known to be important for development, growth and organogenesis, and dysregulation of this pathway leads to tumor progression. We and others find that YAP is up-regulated in human gliomas and associated with worse prognosis of patients. However, the role and mechanism of YAP in glioma progression is largely unknown. Methods: The expression of YAP in glioma tissues was detected by quantitative polymerase chain reaction (qPCR) and immunoblotting. The effect of YAP on glioma progression was examined using cell growth assays and intracranial glioma model. The effect of YAP on beta-catenin protein level, subcellular location and transcription activity was examined by immunoblotting, immunofluorescence and RT-PCR. Results: Firstly, knockdown of YAP inhibited glioma cell proliferation in vitro and tumor growth in vivo. In addition, YAP modulated the protein level, subcellular location and transcription activity of beta-catenin via regulating the activity of GSK3 beta. Lastly, beta-catenin partially mediated the effect of YAP on glioma cell proliferation. Conclusion: Our findings identify that YAP promotes human glioma growth through enhancing Wnt/beta-catenin signaling. In addition, this study provides a new crosstalk mechanism between Hippo/YAP and Wnt/beta-catenin pathways, which suggests a new strategy for human glioma treatment.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available