Nitidine chloride inhibits G2/M phase by regulating the p53/14-3-3 Sigma/CDK1 axis for hepatocellular carcinoma treatment
Bo Zhang,
Bo Zhou,
Guihong Huang,
Jing'an Huang,
Xiaoxin Lin,
Zonghuai Li,
Yuanchu Lian,
Qiujie Huang,
Yong Ye
Affiliations
Bo Zhang
Scientific Research Center, Guilin Medical University, Guilin, China
Bo Zhou
Scientific Research Center, Guilin Medical University, Guilin, China
Guihong Huang
Department of Pharmacy, The Second Affiliated Hospital of Guilin Medical University, Guilin, China; Guangxi Health Commission Key Laboratory of Glucose and Lipid Metabolism Disorders, Key Laboratory of Diabetic Systems Medicine, The Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, 541199, China; Guangxi Key Laboratory of Drug Discovery and Optimization, Guangxi Engineering Research Center for Pharmaceutical Molecular Screening and Druggability Evaluation, School of Pharmacy, Guilin Medical University, Guilin, Guangxi, 541199, China
Jing'an Huang
Scientific Research Center, Guilin Medical University, Guilin, China
Xiaoxin Lin
Scientific Research Center, Guilin Medical University, Guilin, China
Zonghuai Li
Scientific Research Center, Guilin Medical University, Guilin, China
Yuanchu Lian
Scientific Research Center, Guilin Medical University, Guilin, China
Qiujie Huang
Guangxi University of Chinese Medicine, Teaching Experiment and Training Center, Nanning, China; Corresponding author.
Yong Ye
School of Pharmacy, Guangxi Medical University, Guangxi, China; Guangxi Key Laboratory of Bioactive Molecules Research and Evaluation, China; Corresponding author. School of Pharmacy, Guangxi Medical University, Guangxi, China.
Background: Liver cancer had become the sixth most common cancer. Nitidine chloride (NC) has demonstrated promising anti-HCC properties; however, further elucidation of its mechanism of action is necessary. Methods: The anti-HCC targets of NC were identified through the utilization of multiple databases and ChIPs data analysis. The GO and KEGG analyses to determine the specific pathway affected by NC. The Huh 7 and Hep G2 cells were subjected to a 24-h treatment with NC, followed by evaluating the impact of NC on cell proliferation and cell cycle. The involvement of the p53/14-3-3 Sigma/CDK1 axis in HCC cells was confirmed by qPCR and WB analysis of the corresponding genes and proteins. Results: The GO and KEGG analysis showed the targets were related to cell cycle and p53 signaling pathways. In vitro experiments showed that NC significantly inhibited the proliferation of HCC cells and induced G2/M phase arrest. In addition, qPCR and WB experiments showed that the expression of p53 in HCC cells increased after NC intervention, while the expression of 14-3-3 Sigma and CDK1 decreased. Conclusion: NC can inhibit the proliferation of HCC cells and induce G2/M cell cycle arrest, potentially by regulating the p53/14-3-3 Sigma/CDK1 axis.
