Imperial College London
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Dr. Jia Li

Faculty of Medicine, Department of Metabolism, Digestion and Reproduction

Reader in Biological Chemistry
 
 
 
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Contact

 

+44 (0)20 7594 3230jia.li

 
 
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Location

 

10.N2ACommonwealth BuildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Hu:2021:10.1016/j.jare.2020.12.007,
author = {Hu, C and Iwasaki, M and Liu, Z and Wang, B and Li, X and Lin, H and Li, J and Li, JV and Lian, Q and Ma, D},
doi = {10.1016/j.jare.2020.12.007},
journal = {Journal of Advanced Research},
pages = {1--12},
title = {Lung but not brain cancer cell malignancy inhibited by commonly used anesthetic propofol during surgery: Implication of reducing cancer recurrence risk},
url = {http://dx.doi.org/10.1016/j.jare.2020.12.007},
volume = {31},
year = {2021}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - IntroductionIntravenous anesthesia with propofol was reported to improve cancer surgical outcomes when compared with inhalational anesthesia. However, the underlying molecular mechanisms largely remain unknown.ObjectivesThe anti-tumor effects of propofol and the possible underlying mechanism including altered metabolic and signaling pathways were studied in the current study.MethodsThe cell viability, proliferation, migration, and invasion of cancer cells were analyzed with CCK-8, Ki-67 staining, wound healing, and Transwell assay, respectively. The protein changes were analyzed with Western blot and immunofluorescent staining. The metabolomics alteration was studied with 1H-NMR spectroscopy. The gene expression regulations were analyzed with PCR gene array and qRT-PCR experiments.ResultsIn this study, we found that propofol reduced cell viability and inhibited cell proliferation, migration and invasion of lung cancer cells, but not neuroglioma cells. In lung cancer cells, propofol downregulated glucose transporter 1 (GLUT1), mitochondrial pyruvate carrier 1 (MPC1), p-Akt, p-Erk1/2, and hypoxia- inducible factor 1 alpha (HIF-1 α ) expressions and upregulated pigment epithelium-derived factor (PEDF) expression. Propofol increased intracellular glutamate and glycine but decreased acetate and formate whilst increased glucose, lactate, glutamine, succinate, pyruvate, arginine, valine, isoleucine, and leucine and glycerol, and decreased acetate, ethanol, isopropanol in the culture media of lung cancer cells. Furthermore, VEGFA, CTBP1, CST7, CTSK, CXCL12, and CXCR4 gene expressions were downregulated, while NR4A3, RB1, NME1, MTSS1, NME4, SYK, APC, and FAT1 were upregulated following the propofol treatment. Consistent with the phenotypical changes, these molecular and metabolic changes were not found in the neuroglioma cells.ConclusionOur findings indicated anti-tumor effects of propofol on the lung cancer but not brain cancer, through the regulation of tumor metasta
AU  - Hu,C
AU  - Iwasaki,M
AU  - Liu,Z
AU  - Wang,B
AU  - Li,X
AU  - Lin,H
AU  - Li,J
AU  - Li,JV
AU  - Lian,Q
AU  - Ma,D
DO  - 10.1016/j.jare.2020.12.007
EP  - 12
PY  - 2021///
SN  - 2090-1232
SP  - 1
TI  - Lung but not brain cancer cell malignancy inhibited by commonly used anesthetic propofol during surgery: Implication of reducing cancer recurrence risk
T2  - Journal of Advanced Research
UR  - http://dx.doi.org/10.1016/j.jare.2020.12.007
UR  - https://www.sciencedirect.com/science/article/pii/S2090123220302575?via%3Dihub
UR  - http://hdl.handle.net/10044/1/85775
VL  - 31
ER  -
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