Oncotarget

Research Papers:

Retinol dehydrogenase-10 promotes development and progression of human glioma via the TWEAK-NF-κB axis

Feng Guan, Liang Wang, Shuyu Hao, Zhen Wu, Jian Bai, Zhuang Kang, Quan Zhou, Hong Chang, Hui Yin, Da Li, Kaibin Tian, Junpeng Ma, Guijun Zhang and Junting Zhang _

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Oncotarget. 2017; 8:105262-105275. https://doi.org/10.18632/oncotarget.22166

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Abstract

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

Correspondence to:

Junting Zhang, email: [email protected]

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

ABSTRACT

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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