Inhibition of the expression of a proliferation-induced ligand APRIL in HepG2 cell line and the reversal on tumor immune evasion by Chinese medicine

Authors

  • Shi-Hai Kan Department of Human Anatomy, Binzhou Medical University, 346 Guanhai Road, Yantai
  • Jing Tang Department of Laboratory Medicine, Yantai Economic and Techno-logical Development Zone Hospital, Yantai
  • Du-Jun Li Department of Laboratory Medicine, Yantai Economic and Techno-logical Development Zone Hospital, Yantai
  • Zhi-Qiang Wang Department of Human Anatomy, Binzhou Medical University, 346 Guanhai Road, Yantai
  • Chun-Xia Li Department of immunology, Jining Medical University, Jining
  • Fei Huang Department of Human Anatomy, Binzhou Medical University, 346 Guanhai Road, Yantai,

DOI:

https://doi.org/10.3329/bjp.v7i4.11888

Keywords:

ADM, Baicali, Cell proliferation, Icarrin, Tumor, Tumor immune evasion

Abstract

This study was designed to examine the role and mechanism of ICA, Baicali in combination with ADM on inhibiting the expression of APRIL in HepG2 cells. MTT assay was used to explore tumor cells proliferation and cytotoxic activity. RT-PCR was used to examine the expression level of APRIL, its receptor HSPG and apoptosis-associated gene bcl-2. ICA, Baicali and ADM can significantly inhibit the proliferation activity of HepG2 cells in a time-dependent manner, and this inhibition of cell proliferation was time dependent; APRIL and its receptor HSPG were strongly expressed on HepG2 cells. In conclusion, by inhibiting the expression of bcl-2 on HepG2 cells, ICA, Baicali and ADM could significantly enhance the susceptibility of HepG2 cells to lysis by CD3AK , reverse tumor immune evasion.

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Published

2012-10-15

How to Cite

Kan, S.-H., J. Tang, D.-J. Li, Z.-Q. Wang, C.-X. Li, and F. Huang. “Inhibition of the Expression of a Proliferation-Induced Ligand APRIL in HepG2 Cell Line and the Reversal on Tumor Immune Evasion by Chinese Medicine”. Bangladesh Journal of Pharmacology, vol. 7, no. 4, Oct. 2012, pp. 236-42, doi:10.3329/bjp.v7i4.11888.

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Section

Research Articles