Journal
ONCOTARGET
Volume 8, Issue 62, Pages 105262-105275Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.22166
Keywords
retinol dehydrogenase 10 (RDH10); glioma; the cancer genome atlas (TCGA); tumor necrosis factor-like weak inducer of apoptosis (TWEAK); nuclear factor kapaB (NF-kappa B)
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Funding
- Research Special Fund for Public Welfare Industry of Health of China [201402008]
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Retinol dehydrogenase-10 (RDH10) is a member of the short-chain dehydrogenase/reductase family, which plays an important role in retinoic acid (RA) synthesis. Here, we show that RDH10 is highly expressed in human gliomas, and its expression correlates with tumor grade and patient survival times. In vitro, lentivirus-mediated shRNA knockdown of RDH10 suppressed glioma cell proliferation, survival, and invasiveness and cell cycle progression. In vivo, RDH10 knockdown reduced glioma growth in nude mice. Microarray analysis revealed that RDH10 silencing reduces expression of TNFRSF12A (Fn14), TNFSF12 (TWEAK), TRAF3, IKBKB (IKK-beta), and BMPR2, while it increases expression of TRAF1, NFKBIA (I kappa B alpha), NFKBIE (I kappa B epsilon), and TNFAIP3. This suggests that RDH10 promotes glioma cell proliferation and survival by regulating the TWEAK-NF-kappa B axis, and that it could potentially serve as a novel target for human glioma treatment.
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