Xiaoai Jiedu Recipe Inhibits Proliferation and Metastasis of Non-Small Cell Lung Cancer Cells by Blocking the P38 Mitogen-Activated Protein Kinase (MAPK) Pathway

被引:13
作者
Wang, Yuchao [1 ,2 ]
Xu, Chunhua [2 ]
Xu, Bin [1 ,3 ]
Li, Li [4 ]
Li, Wenting [4 ]
Wang, Wei [2 ]
Wu, Mianhua [4 ]
机构
[1] Nanjing Univ Chinese Med, Nanjing, Jiangsu, Peoples R China
[2] Nanjing Chest Hosp, Endoscop Ctr, Nanjing, Jiangsu, Peoples R China
[3] Nanjing Chest Hosp, Dept Resp Med, Nanjing, Jiangsu, Peoples R China
[4] Nanjing Univ Chinese Med, Inst Oncol, Clin Med Coll 1, Nanjing, Jiangsu, Peoples R China
来源
MEDICAL SCIENCE MONITOR | 2019年 / 25卷
关键词
Apoptosis; Carcinoma; Non-Small-Cell Lung; Cell Proliferation; MAP Kinase Signaling System; DECOCTION; APOPTOSIS; MIGRATION; INVASION; CYCLE;
D O I
10.12659/MSM.917115
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background: Lung cancer is the leading cause of cancer deaths in the world. Its major histopathological subtype is non-small cell lung cancer (NSCLC). Xiaoai Jiedu recipe (XJR) is a traditional Chinese medicine formula that can suppress growth and invasion of tumor cells. Here, we assessed the antitumor effect of XJR on NSCLC explored the underlying mechanisms. Material/Methods: Three concentrations of XJR (low, middle, and high) were used to treat A549 cells. Cell Counting Kit-8 and colony formation assay were used to measure proliferation of A549 cells. Apoptosis was evaluated by Hoechst 33342 staining and flow cytometry. The expression of apoptosis-associated proteins was measured by Western blot analysis. Transwell and scratch wound healing assay were used to assess invasion and migration, respectively, of A549 cells. The expression of p38 MAPK pathway-associated proteins were measured using Western blot analysis. Results: XJR suppressed proliferation and promoted apoptosis of A549 cells, especially in the high-dose group. The expression of Bcl-2 was reduced with increasing expression of Bax, cleaved caspase-3, and cleaved caspase-9. Invasion and migration abilities of A549 cells were inhibited after XJR treatment. XJR treatment decreased the expression levels of phosphorylated p38 (p-p38), p-ERK, and p-JNK in a dose-dependent manner. Conclusions: The results demonstrated that XJR can inhibit proliferation, invasion, and migration, and induce apoptosis of NSCLC by blocking the p38 MAPK pathway, which shows the potential of XJR as a new treatment of NSCLC.
引用
收藏
页码:7538 / 7546
页数:9
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