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ISSN 2097-3497 (Online)
CN 22-1108/R
Volume 40 Issue 6
Jun.  2024
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Article Contents

Effect of iridoid glycosides from Boschniakia rossica on epithelial-mesenchymal transition of HepG2 cells induced by transforming growth factor-beta 1

DOI: 10.12449/JCH240617
Research funding:

National Natural Science Foundation of China (82060113);

National Natural Science Foundation of China (81760659);

Jilin Province Education Department project (JJKH20210578KJ)

More Information
  • Corresponding author: QUAN Jishu, quanjs@ybu.edu.cn (ORCID: 0000-0002-6466-5787)
  • Received Date: 2024-01-23
  • Accepted Date: 2024-02-28
  • Published Date: 2024-06-25
  •   Objective  To investigate the effect of iridoid glycosides from Boschniakia rossica (IGBR) on epithelial-mesenchymal transition (EMT) of HepG2 hepatoma cells induced by transforming growth factor-beta 1 (TGF-β1).  Methods  HepG2 hepatoma cells were induced by 10 μg/L TGF-β1 to construct an EMT model of hepatoma cells. The cells were divided into control group (treated with serum-free DMEM), model group (treated with 10 μg/L TGF-β1), and IGBR group (treated with 10 μg/L TGF-β1 and 500 mg/L IGBR), and all cells were cultured for 48 hours. Cell adhesion assay, wound healing assay, and Transwell chamber assay were used to observe the migration and invasion abilities of cells. RT-PCR and Western blot were used to measure the mRNA and protein expression levels of E-cadherin, N-cadherin, and vimentin in cells, and Western blot was used to measure the protein expression levels of Slug, Twist1, ZEB1, p-STAT3, and STAT3. A one-way analysis of variance was used for comparison of continuous data between multiple groups, and the least significant difference t-test was used for further comparison between two groups; the independent-samples t test was used for comparison between two groups.  Results  After TGF-β1 induction, HepG2 cells in the model group showed long spindle-shape changes, while those in the control group showed polygonal epithelia-like changes. Compared with the model group, the IGBR group had a significant reduction in cell adhesion rate and significant inhibition of cell migration and invasion abilities (all P<0.05), as well as significant increases in the mRNA and protein expression levels of E-cadherin (P<0.05), significant reductions in the mRNA and protein expression levels of N-cadherin and vimentin (all P<0.05), and significant reductions in the protein expression levels of Slug, Twist1, ZEB1, and p-STAT3 (all P<0.05).  Conclusion  IGBR can inhibit TGF-β1-induced EMT process in HepG2 cells, thereby attenuating cell adhesion, migration, and invasion abilities, and it can also upregulate E-cadherin, downregulate N-cadherin and vimentin, and upregulate the protein expression of Slug, Twist1, ZEB1, and STAT3, possibly by inhibiting the STAT3 pathway to downregulate the EMT transcription factors such as Slug, Twist1, and ZEB1.

     

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