Journal
ONCOTARGET
Volume 8, Issue 9, Pages 14343-14358Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.11102
Keywords
gliblastoma; EMP3; TGF-beta; TGFBR2; tumorigenesis
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Funding
- National Natural Science Foundation of China [81500717, 81372792, 81372685]
- Key Projects in the National Science & Technology Pillar Program during the Twelfth Five-year Plan Period [2014BAI04B02]
- Chinese Society of Neuro-Oncology (CSNO) research project [CSNO-2015-MSD13]
- China Postdoctoral Science Foundation
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Although epithelial membrane protein 3 (EMP3) has been implicated as a candidate tumor suppressor gene for low grade glioma, its biological function in glioblastoma multiforme (GBM) still remains poorly understood. Herein, we showed that EMP3 was highly expressed in CD44-high primary GBMs. Depletion of EMP3 expression suppressed cell proliferation, impaired in vitro tumorigenic potential and induced apoptosis in CD44-high GBM cell lines. We also identified TGF-beta/Smad2/3 signaling pathway as a potential target of EMP3. EMP3 interacts with TGF-beta receptor type 2 (TGFBR2) upon TGF-beta stimulation in GBM cells. Consequently, the EMP3TGFBR2 interaction regulates TGF-beta/Smad2/3 signaling activation and positively impacts on TGF-beta-stimulated gene expression and cell proliferation in vitro and in vivo. Highly correlated protein expression of EMP3 and TGF-beta/Smad2/3 signaling pathway components was also observed in GBM specimens, confirming the clinical relevancy of activated EMP3/TGF-beta/Smad2/3 signaling in GBM. In conclusion, our findings revealed that EMP3 might be a potential target for CD44-high GBMs and highlight the essential functions of EMP3 in TGF-beta/Smad2/3 signaling activation and tumor progression.
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