Retinol dehydrogenase-10 promotes development and progression of human glioma via the TWEAK-NF-κB axis
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Feng Guan1, Liang Wang1, Shuyu Hao1, Zhen Wu1, Jian Bai2, Zhuang Kang3, Quan Zhou4, Hong Chang4, Hui Yin5, Da Li1, Kaibin Tian1, Junpeng Ma1, Guijun Zhang1 and Junting Zhang1
1Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
2CAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, China
3Department of Glioma, Beijing Shijitan Hospital, Capital Medical University, Beijing, China
4Department of Pathology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China
5Department of Social Medicine and Health Education, School of Public Health, Peking University, Beijing, China
Junting Zhang, email: email@example.com
Keywords: retinol dehydrogenase 10 (RDH10); glioma; the cancer genome atlas (TCGA); tumor necrosis factor-like weak inducer of apoptosis (TWEAK); nuclear factor kapaB (NF-κB)
Received: February 09, 2017 Accepted: September 25, 2017 Published: October 27, 2017
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-β), and BMPR2, while it increases expression of TRAF1, NFKBIA (IκBα), NFKBIE (IκBε), and TNFAIP3. This suggests that RDH10 promotes glioma cell proliferation and survival by regulating the TWEAK-NF-κB axis, and that it could potentially serve as a novel target for human glioma treatment.
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