Ji Cao

Prof. Ji Cao


Research Focus & Metrics

Academic Career Length

12Years (2015-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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9 March 2020 in Acta Pharmacologica Sinica
Verified
Journal Article
Closed access
PDF file
QWQian Wu
Qian Wu
LJLi Jiang
Li Jiang
SLSi-Cheng Li
Si-Cheng Li
QHQiao-Jun He
Qiao-Jun He
BYBo Yang
Bo Yang
JCJi Cao
Ji Cao

12 January 2018 in Frontiers in Pharmacology
Verified
Journal Article
Open access
BLBin Lu
Bin Lu
XCXiao Bing Chen
Xiao Bing Chen
MYMei Dan Ying
Mei Dan Ying
QHQiao Jun He
Qiao Jun He
JCJi Cao
Ji Cao
BYBo Yang
Bo Yang
Ferroptosis is a process driven by accumulated iron-dependent lipid ROS that leads to cell death, which is a distinct regulated-cell death comparing to other cell death. The lethal metabolic imbalance resulted from GSH depletion or inactivation of glutathione peroxidase 4 (GPX4) is the executor of ferroptosis within the cancer cell. Small molecules-induced ferroptosis has a strong inhibition of tumor growth and enhances the sensitivity of chemotherapeutic drugs, especially in the condition of drug resistance. These evidences have highlighted the importance of ferroptosis in cancer therapeutics, but the roles of ferroptosis in tumorigenesis and development remain unclear. This article provides an overview of the mechanisms of ferroptosis, highlights the role of ferroptosis in cancer and discusses strategies for therapeutic modulation.

28 February 2019 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Open access
PDF file
JCJi Cao
Ji Cao
LSLei Sun
Lei Sun
PAPornpun Aramsangtienchai
Pornpun Aramsangtienchai
NSNicole A. Spiegelman
Nicole A. Spiegelman
XZXiaoyu Zhang
Xiaoyu Zhang
HLHening Lin
Hening Lin
Significance: HDAC11 is the only class IV member of the histone deacetylase (HDAC) family, and very little is known about its biological function. The work here reveals its efficient and physiologically relevant activity. The regulation of SHMT2 and interferon signaling expands the known biological function of protein lysine fatty acylation, which has only recently started to be appreciated. Furthermore, a compelling molecular mechanism is proposed to connect HDAC11 to immune response. The finding opens exciting opportunities to develop HDAC11-specific inhibitors to treat human diseases that would benefit from increased type I interferon signaling, such as viral infection, multiple sclerosis, and cancer.

29 April 2019 in Acta Pharmacologica Sinica
Verified
Journal Article
Closed access
PDF file
BLBin Lu
Bin Lu
XCXiao-Bing Chen
Xiao-Bing Chen
YHYu-Cai Hong
Yu-Cai Hong
HZHong Zhu
Hong Zhu
QHQiao-Jun He
Qiao-Jun He
JCJi Cao
Ji Cao

23 February 2024 in Science Advances
Verified
Journal Article
Open access
LLLi Lu
Li Lu
MXMingqi Xie
Mingqi Xie
BYBo Yang
Bo Yang
ZWZhao Wenbin
Zhao Wenbin
JCJi Cao
Ji Cao
Chimeric antigen receptor T (CAR-T) cell therapy is a promising and precise targeted therapy for cancer that has demonstrated notable potential in clinical applications. However, severe adverse effects limit the clinical application of this therapy and are mainly caused by uncontrollable activation of CAR-T cells, including excessive immune response activation due to unregulated CAR-T cell action time, as well as toxicity resulting from improper spatial localization. Therefore, to enhance controllability and safety, a control module for CAR-T cells is proposed. Synthetic biology based on genetic engineering techniques is being used to construct artificial cells or organisms for specific purposes. This approach has been explored in recent years as a means of achieving controllability in CAR-T cell therapy. In this review, we summarize the recent advances in synthetic biology methods used to address the major adverse effects of CAR-T cell therapy in both the temporal and spatial dimensions.

18 March 2020 in Acta Pharmacologica Sinica
Verified
Journal Article
Closed access
PDF file
MYMeng Yuan
Meng Yuan
ZSZi-Han Song
Zi-Han Song
MYMei-Dan Ying
Mei-Dan Ying
HZHong Zhu
Hong Zhu
QHQiao-Jun He
Qiao-Jun He
JCJi Cao
Ji Cao