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Huarong Chen

As seen in: Nature, Wiley Online Library, Gut Journal, MDPI, Science Magazine, Cell Metabolism, Gastroenterology
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Articles

Compartmentalized branched-chain amino acid metabolism orchestrates colorectal cancer dissemination via an UMP-vimentin axis

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By Fenfen Ji, Pingmei Huang, Qiming Zhou, Qinyao Wei, Charis Chan, Danyu Chen, Huarong Chen, WEI KANG, Alvin Ho-Kwan Cheung, Yasi Pan, Ying Jiao, Lin Zhu Verified, Peisi Xie, Xiao Liang, Onno Kranenburg, Zongwei Cai, Jun Yu, Lok Hin Ko, Cillian H. Cheng, Jianming Shen, Tat Wai Chik, Lok Hin Ko, Cillian H. Cheng, Jianming Shen, Tat Wai Chik, Onno Kranen
| Cell Metabolism Verified
ArticleVolume 38, Issue 4p794-811.e8Open access Affiliations & Notes 1Institute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China 2Department of Anaesthesia, Intensive Care and Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China 3Department of Anatomical and Cellular Pathology, The Chinese...
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Strand-asymmetric G-runs and G4s downstream of TSS modulate tumor suppressor gene transcription

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By Dan Huang, Xiaoting Zhang, Xiansong Wang, Ziheng Huang, Judeng Zeng, Xiaodong Liu, Likai Tan, Lin Zhang, Zhenxing Guo, Tony Gin, Jun Yu, Kwok M. Ho, Huarong Chen
| Nature Verified
Abstract A genome sequence is not made up of random nucleotides. Instead, it has distinctive features for evolutionary adaptation. Herein, we identified a higher frequency of continuous guanines (G-runs) located downstream of the transcription start site (TSS) in the non-template strand than that of the template strand by analyzing the genomic region around TSS (TSS ± 1 kb) across different species. G-runs are known to have the propensity to form G-quadruplex structures (G4).
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YTHDF1 targets the chemotherapy response by suppressing NOTCH1-induced stemness in colorectal cancer - Signal Transduction and Targeted Therapy

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By Henley Cheung, Huarong Chen, Weixin Liu, WEI KANG, Ka-Fai To, Housheng Hansen He
| Nature Verified
Abstract N6-methyladenosine (m6A) modification of mRNAs is a predominant epigenetic regulatory mechanism in tumor initiation and progression. Cancer stem cells (CSCs) are the key drivers of colorectal cancer (CRC) initiation and chemotherapy resistance. Here, we found that the m6A reader YT521-B homologous domain family, member 1 (YTHDF1), promotes CRC stemness, tumorigenesis, and chemotherapy resistance.
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