Quantitative Proteomics Based on iTRAQ Reveal that Nitidine Chloride Induces Apoptosis by Activating JNK/c-Jun Signaling in Hepatocellular Carcinoma Cells
Planta Med DOI: 10.1055/a-1676-4307The aim of the present study was to investigate the cytotoxic effects and
underlying molecular mechanisms of nitidine chloride (NC) in hepatocellular
carcinoma cells via quantitative proteomics. MTT assays were used to detect the
inhibitory effects of NC in Bel-7402 liver cancer cells, and the number of
apoptotic cells was measured by flow cytometry. Quantitative proteomics
technology based on iTRAQ was used to discover differential expressed proteins
after NC treatment, and bioinformatic techniques were further used to screen
potential targets of NC. Molecular docking was applied to evaluate the docking
activity of NC with possible upstream proteins, and their expression was
detected at the mRNA and protein levels by quantitative reverse transcription
PCR and western blotting. NC inhibited the proliferation of Bel-7402 cells after
24 h of treatment and stimulated apoptosis in vitro. The proteomics
experiment showed that NC triggers mitochondrial damage in HCC cells and
transcription factor AP-1 (c-Jun) may be a potential target of NC (fold
change = 4.36 ± 0.23). Molecular docking results revealed the highest docking
score of NC with c-Jun N-terminal kinase (JNK), one of the upstream proteins of
c-Jun. Moreover, the mRNA and protein expression of c-Jun and JNK were
significantly increased after NC treatment (p < 0.05). These findings
i...
Source: Planta Medica - Category: Drugs & Pharmacology Authors: Chen, Shipeng Liao, Yinan Lv, Jinyan Hou, Huaxin Feng, Jie Tags: Original Papers Source Type: research
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