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Journal of Zhejiang University SCIENCE B 1998 Vol.-1 No.-1 P.

http://doi.org/10.1631/jzus.B2200038


Investigation and experimental validation of curcumin-related mechanisms against hepatocellular carcinoma based on network pharmacology


Author(s):  Yang CHEN, Qian LI, Sisi REN, Ting CHEN, Bingtao ZHAI, Jiangxue CHENG, Xiaoyan SHI, Liang SONG, Yu FAN, Dongyan GUO

Affiliation(s):  College of Basic Medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China; more

Corresponding email(s):   2111006@sntcm.edu.cn, xmc2051080@163.com

Key Words:  Curcumin, Network Pharmacology, p53, AMPK, Apoptosis, Autophagy


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Yang CHEN, Qian LI, Sisi REN, Ting CHEN, Bingtao ZHAI, Jiangxue CHENG, Xiaoyan SHI, Liang SONG, Yu FAN, Dongyan GUO. Investigation and experimental validation of curcumin-related mechanisms against hepatocellular carcinoma based on network pharmacology[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .

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volume="-1",
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year="1998",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2200038"
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Abstract: 
To determine the potential molecular mechanisms underlying the therapeutic effect of curcumin on hepatocellular carcinoma (HCC) by network Pharmacology and experimental in vitro validation. Methods: The predictive targets of curcumin or HCC were collected from several databases. The identified overlapping targets were crossed with gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis using The Database for Annotation, Visualization and Integrated Discovery (DAVID) platform. Two of the candidate pathways were selected to conduct an experimental verification. MTT assay was used to determine the effect of curcumin on the viability of HepG2 and LO2 cells. The apoptosis and autophagy of HepG2 cells were respectively detected by flow cytometry and transmission electron microscope. Besides, western blot and real-time PCR were employed to verify the p53 apoptotic pathway and Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) autophagy pathway. HepG2 cells were pretreated with pifithrin-α (PFT-α) and GSK690693 for further investigation. Results: The 167 pathways analyzed by KEGG included apoptosis, autophagy, p53, and AMPK pathway. The GO enrichment analysis demonstrated that curcumin was involved in cellular response to drug, regulation of apoptotic pathway, and so on. The in vitro experiments also confirmed that curcumin can inhibit the growth of HepG2 cells by promoting the apoptosis of p53 pathway and autophagy through the AMPK pathway. Furthermore, the protein and message RNA (mRNA) of the two pathways were downregulated in the inhibitor-pretreated group compared with the experimental group. The damage-regulated autophagy modulator (DRAM) in the PFT-α-pretreated group was downregulated, and p62 in the GSK690693-pretreated group was upregulated. Conclusion: curcumin can treat HCC through the p53 apoptotic pathway and the AMPK/ULK1 autophagy pathway, in which the mutual transformation of autophagy and apoptosis may occur through DRAM and p62.

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