Honokiol Suppression of Human Epidermal Growth Factor Receptor 2 (HER2)-Positive Gastric Cancer Cell Biological Activity and Its Mechanism
Author(s) -
YiDan Yan,
Jianmin Xu,
Guoxin Mao
Publication year - 2020
Publication title -
medical science monitor
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.636
H-Index - 85
eISSN - 1643-3750
pISSN - 1234-1010
DOI - 10.12659/msm.923962
Subject(s) - honokiol , pi3k/akt/mtor pathway , protein kinase b , cell growth , cell cycle , microbiology and biotechnology , apoptosis , biology , epidermal growth factor , cell , cancer cell , chemistry , cancer research , cancer , receptor , pharmacology , biochemistry , genetics
BACKGROUND The purpose of our study was to determine the effects and mechanisms of honokiol on human epidermal growth factor receptor 2 (HER2)-positive gastric cancer cells by in vitro study. MATERIAL AND METHODS We measured HER2 expression in different gastric cancer cell lines by real-time quantitative polymerase chain reaction (RT-qPCR) and western blot (WB) assay. Cell proliferation, apoptosis, and cell cycle were evaluated by cell-counting kit 8 and flow cytometry assays. The invading cell numbers and wound-healing rates were measured by transwell and wound-healing assays. Phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), P21, and matrix metalloproteinase (MMP)-9 proteins and messenger ribonucleic acid (mRNA) expression were measured by WB and RT-qPCR assay. HER2 protein expression was evaluated by cellular immunofluorescence. RESULTS Honokiol suppressed cell proliferation via increasing cell apoptosis, invasion, and migration with dose dependence. By WB and RT-qPCR assays, compared with the control group, PI3K, AKT, P21, and MMP-9 proteins and mRNA expression were significantly different (P<0.05). By cellular immunofluorescence, HER2 protein expression was significantly depressed in honokiol-treated groups compared with control groups (P<0.05). CONCLUSIONS Honokiol has suppressive effects on HER2-positive gastric cancer cell biological activities via regulation of HER2/PI3K/AKT pathways in vitro.
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