2. Academic Validation
  3. Emodin inhibits invasion and migration of hepatocellular carcinoma cells via regulating autophagy-mediated degradation of snail and β-catenin

Emodin inhibits invasion and migration of hepatocellular carcinoma cells via regulating autophagy-mediated degradation of snail and β-catenin

  • BMC Cancer. 2022 Jun 18;22(1):671. doi: 10.1186/s12885-022-09684-0.
Binyu Qin  # 1 2 3,  Zhili Zeng  # 1 2 3,  Jianliang Xu  # 4,  Jing Shangwen 2,  Zeng Jie Ye 3,  Shutang Wang 5,  Yanheng Wu 6,  Gongfeng Peng 6,  Qi Wang 7,  Wenyi Gu 8 9,  Ying Tang 10 11 12
Affiliations

Affiliations

  • 1 Institute of Tumor, Guangzhou University of Chinese Medicine, Guangzhou, China.
  • 2 Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
  • 3 Guangzhou University of Chinese Medicine, Guangzhou, China.
  • 4 Hepatobilliary Surgery Department, The Third affiliated Hospital of Su Yat-sen University, Guangzhou, China.
  • 5 Department of Oncology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China.
  • 6 Gillion ITM Research Institute, Guangzhou Hongkeyuan, Guangzhou, China.
  • 7 Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China. wangqi@gzucm.edu.cn.
  • 8 Gillion ITM Research Institute, Guangzhou Hongkeyuan, Guangzhou, China. w.gu@uq.edu.au.
  • 9 Australian Institute of Bioengineering and Nanotechnology, The University of Queensland, QLD, Brisbane, 4072, Australia. w.gu@uq.edu.au.
  • 10 Institute of Tumor, Guangzhou University of Chinese Medicine, Guangzhou, China. tangying@gzucm.edu.cn.
  • 11 Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China. tangying@gzucm.edu.cn.
  • 12 Guangzhou University of Chinese Medicine, Guangzhou, China. tangying@gzucm.edu.cn.
  • # Contributed equally.
PMID: 35715752 DOI: 10.1186/s12885-022-09684-0
Abstract

Background: Previous studies reported that emodin extracted from Rheum palmatum L. exerts antiproliferation and antimetastatic effects in a variety of human Cancer types. However, the role of emodin in hepatocellular carcinoma (HCC) remain unknown.

Methods: EdU and colony formation assays were performed to evaluate the effects of emodin on proliferation. The mobility capacities of HCC treated with emodin were evaluated using wound healing assay. Transwell invasion and migration assays were performed to evaluate anti-migratory and anti-invasive effects of emodin on HCC. Annexin V-FITC/PI was performed to analyze the Apoptosis. PI stain was performed to analyze cell cycle. RNA Sequencing technology was used to identify the differentially expressed genes (DEGs) induced by emodin in HCC. The impact of emodin on autophagic flux in HepG2 cells was examined by mCherry-GFP-LC3 analysis. Western blot was used to assess the protein expressions of epithelial-mesenchymal transition (EMT), Autophagy, PI3K/Akt/mTOR and Wnt/β-catenin signaling pathway.

Results: We found that emodin inhibited the growth of HepG2 cells in a dose- and time-dependent manner. In addition, emodin inhibited cell proliferation, induced S and G2/M phases arrest, and promoted Apoptosis in HepG2 cells. The migration and invasion of HepG2 cells were also suppressed by emodin. Enrichment analysis revealed that DEGs involved in cell adhesion, Cancer metastasis and cell cycle arrest. Moreover, western bolt results show that emodin-induced Autophagy promotes Snail and β-catenin degradation. We also found that blocking autophagic flux after emodin treatment caused EMT reversal. Furthermore, the PI3K agonist Y-P 740 significantly reversed the phosphorylation levels of GSK3β and mTOR. These results indicated that emodin induced Autophagy and inhibited the EMT in part through suppression of the PI3K/Akt/mTOR and Wnt/β-catenin pathways.

Conclusion: Our study indicated that emodin inhibited cell metastasis in HCC via the crosstalk between Autophagy and EMT.

Keywords

Autophagy; Emodin; Epithelial-mesenchymal transition; Hepatocellular carcinoma; PI3K/AKT/mTOR; Wnt/β-catenin.

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