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Xiuying Xiao

As seen in: Nature, Cell Reports, Cell Metabolism
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Articles

Microbial metabolite FAD mobilizes adipocyte lipid remodeling to enhance cancer immunotherapy efficacy

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By Tianying Tong, Xiaowen Huang, Lingxi Li, Muni Hu, Xiaoqiang Zhu, Beiyao Zhu, Yanru Ma, Lijun Ning, Yi Jiang, Yue Zhang, Yilu Zhou, Zhenyu Wang, Jinmei Ding, Ying Zhao, Baoqin Xuan, Youwei Zhang, Xiuying Xiao, Jing-Yuan Fang, Jie Hong, Yan Yin, Fenglin Liu, Haoyan Chen
| Cell Metabolism Verified
Keywords gut microbiota immunotherapy adipocyte obesity microbial metabolite unsaturated fatty acids Get full text access Log in, subscribe or purchase for full access. References 1. Kwon, S.Y. ∙ Thi-Thu Ngo, H. ∙ Son, J. ... Exploiting bacteria for cancer immunotherapy Nat. Rev. Clin. Oncol. 2024; 21:569-589 2. Ratiner, K. ∙ Ciocan, D. ∙ Abdeen, S.K. ... Utilization of the microbiome in personalized medicine Nat. Rev. Microbiol. 2024; 22:291-308 3. Trefny, M.P. ∙ Kroemer, G. ∙ Zitvogel, L. ...
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NSD2 inhibits the expression of PD-L1 via oxidative phosphorylation to control immune surveillance in hepatocellular carcinoma - Cell Death & Disease

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By Wei Zhang, Wenxin Feng, Chunxiao Ma, Hanyu Rao, Changwei Liu, Yue Xu, Ningyuan Liu, Ziyi WANG, Rebiguli Aji, Ting Han, Wei-Qiang Gao, Xiuying Xiao
| Nature Verified
Abstract Hepatocellular carcinoma (HCC) is the fourth most common cause of cancer-related death, and patients usually exhibit impaired immune function within the tumor environment. NSD2 is an H3K36 methyltransferase and has been considered a cancer-promoting factor. However, the role of NSD2 in the occurrence and development of HCC is still unclear. In this study, the effects of NSD2 on HCC were assessed by both mouse and cell models.
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Histone 3 lysine 36 trimethylation by SETD2 shapes an epigenetic landscape in intestinal stem cells to orchestrate lipid metabolism and attenuate cell senescence | Cell Death & Disease

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By Yue Xu, Ziyi WANG, Wenxin Feng, Hanyu Rao, Dehuan Wang, Wei Zhang, Ningyuan Liu, Jiahe Li, Xiuying Xiao, Wei-Qiang Gao, Rebiguli Aji
| Nature Verified
Abstract The self-renewal capacity of intestinal stem cells (ISCs) declines with aging, leading to a loss of homeostasis and an increased susceptibility to intestinal diseases. Despite the established significance of lipid metabolism and epigenetic regulation in ISC function, the molecular mechanisms that connect these processes to aging-related ISC dysfunction remain elusive. Here, we hypothesize that histone 3 lysine 36 trimethylation (H3K36me3) might act as a bridge between these processes.
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