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Jing Zhang

Researcher at Fourth Military Medical University

Publications -  8
Citations -  633

Jing Zhang is an academic researcher from Fourth Military Medical University. The author has contributed to research in topics: PI3K/AKT/mTOR pathway & Mitochondrion. The author has an hindex of 7, co-authored 8 publications receiving 435 citations.

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Increased mitochondrial fission promotes autophagy and hepatocellular carcinoma cell survival through the ROS-modulated coordinated regulation of the NFKB and TP53 pathways.

TL;DR: It is demonstrated that increased mitochondrial fission plays a critical role in regulation of HCC cell survival, which provides a strong evidence for this process as drug target in HCC treatment.
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CD147 reprograms fatty acid metabolism in hepatocellular carcinoma cells through Akt/mTOR/SREBP1c and P38/PPARα pathways.

TL;DR: It is demonstrated that CD147 is a critical regulator of fatty acid metabolism, which provides a strong line of evidence for this molecule to be used as a drug target in cancer treatment.
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CD147 promotes reprogramming of glucose metabolism and cell proliferation in HCC cells by inhibiting the p53-dependent signaling pathway

TL;DR: The role of CD147 in the regulation of the Warburg effect in HCC cells is investigated and it is demonstrated that CD147 is a crucial regulator of glucose metabolism.
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MCUR1-Mediated Mitochondrial Calcium Signaling Facilitates Cell Survival of Hepatocellular Carcinoma via Reactive Oxygen Species-Dependent P53 Degradation.

TL;DR: This study provides evidence supporting a possible tumor-promoting role for MCUR1-mediated mitochondrial Ca2+ uptake and uncovers a mechanistic understanding that links change of mitochondrial Ca 2+ homeostasis to cancer cell survival, which suggests a potential novel therapeutic target for HCC.
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CD147 promotes liver fibrosis progression via VEGF-A/VEGFR2 signalling-mediated cross-talk between hepatocytes and sinusoidal endothelial cells.

TL;DR: A novel functional mechanism that CD147 may promote liver fibrosis progression via inducing the VEGF-A/VEGFR-2 signalling pathway-mediated cross-talk between hepatocytes and SECs is suggested.