Kang-Ai Injection Inhibits Gastric Cancer Cells Proliferation through IL-6/STAT3 Pathway.
10.1007/s11655-020-3265-6
- Author:
Chun-Lei ZHENG
1
;
Ke-Zuo HOU
1
;
An-Qi WANG
1
;
Wan-Xia FANG
1
;
Shi-Tong YU
1
;
Jin-E LIANG
1
;
Hai-Yan QI
1
;
Xiu-Juan QU
1
;
Yun-Peng LIU
1
;
Xiao-Fang CHE
2
Author Information
1. Department of Medical Oncology, The First Hospital of China Medical University, Shenyang, 110001, China.
2. Department of Medical Oncology, The First Hospital of China Medical University, Shenyang, 110001, China. xfche@cmu.edu.cn.
- Publication Type:Journal Article
- Keywords:
Chinese herbal medicine;
G1 arrest;
Kang-Ai Injection;
gastric cancer;
interleukin-6;
signal transducer and activator of transcription 3
- MeSH:
Apoptosis;
Cell Line, Tumor;
Cell Proliferation;
Cyclin D1/pharmacology*;
Humans;
Interleukin-6/metabolism*;
RNA, Messenger/metabolism*;
STAT3 Transcription Factor/metabolism*;
Stomach Neoplasms/genetics*
- From:
Chinese journal of integrative medicine
2022;28(6):524-530
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To explore the mechanisms underlying the proliferative inhibition of Chinese herbal medicine Kang-Ai injection (KAI) in gastric cancer cells.
METHODS:Gastric cancer cell lines MGC803 and BGC823 were treated by 0, 0.3%, 1%, 3% and 10% KAI for 24, 48 and 72 h, respectively. The cell proliferation was evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. The apoptosis and cell cycle were evaluated by flow cytometry. Interleukin (IL)-6 mRNA and protein expression levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immune sorbent assay (ELISA), respectively. The protein expression levels of cyclin A, cyclin E, cyclin B1, cyclin D1, p21, retinoblastoma (RB), protein kinase B (AKT), extracellular regulated protein kinases (ERK), signal transducer and activator of transcription (STAT) 1 and STAT3 were detected by Western blot.
RESULTS:KAI inhibited the proliferation of MGC803 and BGC823 gastric cancer cells in dose- and time-dependent manner. After treated with KAI for 48 h, the proportion of G1 phase was increased, expression level of cyclin D1 and phosphorylation-RB were down-regulated, whereas the expression of p21 was up-regulated (all P<0.01). Furthermore, 48-h treatment with KAI decreased the phosphorylation level of STAT3, inhibited the mRNA and protein expressions of IL-6 (all P<0.01). IL-6 at dose of 10 ng/mL significantly attenuated the proliferative effect of both 3% and 10% KAI, and recovered KAI-inhibited STAT3 phosphorylation and cyclin D1 expression level (all P<0.01).
CONCLUSION:KAI exerted an anti-proliferative function by inhibiting IL-6/STAT3 signaling pathway followed by the induction of G1 phase arrest in gastric cancer cells.
