Xiongjing

Dr. Jing Xiong obtained her PhD degree at China Pharmaceutical University in a joint PHD program with Mayo Clinic, received a postdoc training at University of Michigan and became a professor at China Pharmaceutical University since 2020. Her group mainly focuses on three aspects regarding liver pathophysiology and drug intervention. Firstly, investigate mechanisms underlying the pathogenesis of metabolic liver diseases, including non-alcoholic fatty liver disease and hepatocellular carcinoma. Secondly, design and develop drugs targeting metabolic homeostasis for the therapy of liver diseases. Thirdly, delineate the mechanisms that regulate the transcription of drug metabolizing enzymes and drug transporters, contributing to the discovery and validation of the potential drug targets for liver injury and reversal of multi-drug resistance.

1、 Educational Experience

2009. 8 – 2010. 9 China Scholarship Council sponsored — Joint PhD program

Mayo Clinic, USA; Supervisor: Virginia M. Miller, PhD, MBA.

2006. 9 – 2011. 7 PhD Degree

China Pharmaceutical University

Major: Pharmacology; Supervisor: Yunman Li

2002. 9 – 2006. 7 Bachelor Degree

Jiangxi Medical University (now affiliated to Nanchang University).

2、Working Experience

2020. 5 – NOW Professor

Department of Pharmacology, School of Pharmacy,

China Pharmaceutical University, China

2017. 8 –2019. 9 Postdoc

Life Sciences Institute, University of Michigan, USA

Supervisor: Jiandie Lin, PhD

2016. 8 – 2020. 4 Associate professor

Department of Pharmacology, School of Basic Medicine,

Nanjing Medical University, China

2011. 8 – 2016. 7 Assistant professor

Department of Pharmacology, School of Basic Medicine,

Nanjing Medical University, China

1、 Yongmei Yin# , Yu Xin, Feng Zhang, Donghao An, Hui Fan, Mengyao Qin, Jinxin Xia, Tao Xi, Jing Xiong*. Overcoming ABCB1-mediated multidrug resistance by transcription factor BHLHE40. Neoplasia. 2023; 39: 100891. IF=6.218

2、Mengyao Qin# , Yu Xin# , Yong Bian# , Xuan Yang, Tao Xi, Jing Xiong*. Phosphorylation- induced ubiquitination and degradation of PXR through

CDK2-TRIM21 axis. Cells. 2022; 11(2):264. IF=7.666

3、Danyu Du# , Chan Liu, Mengyao Qin, Xiao Zhang, Tao Xi, Shengtao Yuan, Haiping Hao*, Jing Xiong*. Metabolic dysregulation and emerging therapeutical

targets for hepato- cellular carcinoma. Acta Pharm Sin B. 2022; 12: 558-580. IF=14.903

4、Jing Xiong* # , Tongyu Liu, Lin Mi, Henry Kuang, Xuelian Xiong, Zhimin Chen, Siming Li, Jiandie D. Lin*. hnRNPU/TrkB defines a chromatin accessibility

checkpoint for liver injury and NASH pathogenesis. Hepatology. 2020; 71: 1228-1246. IF=17.425

5、Tongyu Liu# , Lin Mi# , Jing Xiong, Peter Orchard, Qi Yu, Lei Yu, Xu-Yun Zhao,

Zhuo-Xian Meng, Stephen C. J. Parker, Jiandie D. Lin*, Siming Li*. BAF60a deficiency uncouples chromatin accessibility and cold sensitivity from white fat browning. Nat commun. 2020; 11: 2379. IF=12.121

6、Wenjing Luo# , Yu Xin, Xia Zhao, Feng Zhang, Changqing Liu, Hongwei Fan, Tao Xi*, Jing Xiong*. Suppression of Carboxylesterases by Imatinib Mediated by the Downregulation of Pregnane X Receptor. Br J Pharmacol. 2017; 174(8): 700-717. IF=6.81

7、Xuan Yang# , Xiao Zhang, Yamin Liu, Tao Xi*, Jing Xiong*. Insulin transcriptionally down-regulates carboxylesterases through pregnane X receptor in an Akt-dependent manner. Toxicology. 2019; 422: 60-68. IF=4.099

8、Shujuan Pan# , Yunlong Tan, Shangwu Yao, Yu Xin, Xuan Yang, Jing Liu, Jing Xiong*. Fluoxetine induces lipid metabolism abnormalities by acting on the liver in patients and mice with depression. Acta Pharmacol Sin. 2018; 39(9): 1463-1472. IF=5.064

9、Enfang Shan# , Zhu Zhu, Shuangcheng He, Dongbao Chu, Dinghao Ge, Yunran Zhan, Wei Liu, Jian Yang*, Jing Xiong*. Involvement of Pregnane X Receptor in the suppression of carboxylesterases by metformin in vivo and in vitro, mediated by the activation of AMPK and JNK signaling pathway. Eur J Pharm Sci. 2017; 102: 14-23. IF=5.112

10、Jing Xiong# , Huan Yang, Wenjing Luo, Enfang Shan, Jie Liu, Feng Zhang, Tao Xi*, Jian Yang*. The anti-metastatic effect of 8-MOP on hepatocellular

carcinoma is potentiated by the down-regulation of bHLH transcription factor DEC1. Pharmacol Res. 2016; 105: 121-133. IF=10.334

11、Jing Xiong# , Huan Yang, Lili Wu, Wei Shang, Enfang Shan, Wei Liu, Gang Hu, Tao Xi, Jian Yang*. Fluoxetine suppresses AMP-activated protein kinase

signalingpathway to promote hepatic lipid accumulation in primary mouse hepatocytes. Int J Biochem Cell Bio, 2014; 54: 236–244. IF=5.652

12、Jing Xiong# , Wei Shang, Lili Wu, Ruini Chen, Wei Liu, Rui Ning, Gang Hu, Jian Yang*. Glucose dominates the regulation of carboxylesterases induced by lipopolysaccharide or interleukin-6 in primary mouse hepatocytes. Life sci, Sep 2014; 112: 41–48. IF=6.78

1) National Natural Science Foundation of China (No. 82273982) ：TrkB-T1—Fam83a facilitates liver regeneration through the regulation of liver glucose lipid metabolism and drug screening targeting TrkB-T1, Principal investigator, Jan 2023 to Dec 2026

2) National Natural Science Foundation of China (No. 82070883)：Research on the role and mechanisms of TrkB-T1 promoting the progression of nonalcoholic

steatohepatitis, Principal investigator, Jan 2021 to Dec 2024

3) National Natural Science Foundation of China (No. 81302855)：LPS or IL-6 regulates metabolic nuclear receptor PXR and carboxylesterases, in relation with

drug metabolism disorders in diabetes, Principal investigator, Jan 2014 to Dec 2016

4) Natural Science Foundation of Jiangsu province (No. BK20221525)：Investigating the molecular mechanisms of TrkB-T1 promoting liver regeneration based on the

dynamic regulation of glucose lipid metabolism and drug target validation, Principal investigator, Jul 2022 to Jun 2025

5) Natural Science Foundation of Jiangsu province (No. BK2012446) ：The regulatory actions and mechanisms of SSRIs in liver lipid metabolism, Principal investigator, Jul 2012 to Jun 2015

1) Dr. Jing Xiong mapped the landscape of the transcriptomic reprogramming during metabolic liver injury, especially non-alcoholic fatty liver disease and

hepatocellular carcinoma. Her group revealed that a key nuclear factor hnRNPU mediated NASH pathogenesis. They further investigated a target gene of hnRNPU,

TrkB-T1, which aggravated metabolic injury of hepatocytes and therefore promoted NASH progression. (Hepatology, 2020; Acta Pharm Sin B, 2022)

2) Focusing on the liver adverse reactions caused by drugs, they concealed the underlying mechanisms of drug-associated liver metabolic disorders from clinical,

animal model and cellular perspectives, providing supporting evidence and precedented insights for the clinical rational drug usage. (Acta Pharmacol Sin,

2018; Int J Biochem Cell Bio, 2014)

3) They uncovered the molecular mechanisms of the transcriptional regulation for drug metabolizing enzymes and transporters by focusing on the transcription factors, metabolic nuclear receptors and their target genes, and contributed to the discovery and validation of the potential drug targets for the avoidance and alleviation of drug-induced liver injury, and for the reversal of multi-drug resistance. (Br J Pharmacol, 2017; Toxicology, 2020; Eur J Pharm Sci, 2017; Cells, 2021; Neoplasia, 2022)