Effect of bufalin combined gefitinib on lung cancer H1975 cells and its mechanisms research.
- Author:
Xiao-hong KANG
1
;
Ya-bin GONG
;
Li-fang WANG
;
Zhong-qi WANG
;
Hai-bin DENG
;
Xiao-zhen ZHAO
;
Ji WU
;
Zhen-ye XU
Author Information
- Publication Type:Journal Article
- MeSH: Bufanolides; pharmacology; Carcinoma, Non-Small-Cell Lung; metabolism; pathology; Cell Line, Tumor; Cell Proliferation; drug effects; Drug Synergism; Humans; Lung Neoplasms; metabolism; pathology; Phosphatidylinositol 3-Kinases; metabolism; Proto-Oncogene Proteins c-akt; metabolism; Quinazolines; pharmacology; Receptor, Epidermal Growth Factor; metabolism; Signal Transduction; drug effects
- From: Chinese Journal of Integrated Traditional and Western Medicine 2013;33(8):1081-1085
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of bufalin combined Gefitinib on lung cancer H1975 cells, and to explore its potential mechanisms for anti-tumor.
METHODSThe cytostatic effects of bufalin (1 -100 nmol/L), gefitinib (0.1-20 micromol/L), and bufalin plus gefitinib on H1975 cells were evaluated by MTT assay. Their effects on apoptosis of H1975 cells were determined by flow cytometry (FCM). Their effects on expressions of epidermal growth factor receptor (EGFR) and Met signal pathway related proteins in H1975 cells were detected by Western blot.
RESULTSResults of MTT assay showed that gefitinib over 5 micromol/L could inhibit H1975 cells. But combined therapy of bufalin and gefitinib could potently inhibit the growth of H1975 cells. Results of FCM showed the apoptotic rate was 61.64% +/- 5.61% in the bufalin plus gefitinib group, obviously higher than that of the bufalin group (18.34% +/- 3.42%) and the gefitinib group (7.32% +/- 1.08%), showing statistical difference (P < 0.01). Results of Western blot showed the protein expressions of p-EGFR, p-Met, p-Akt, and p-mTOR in H1975 cells could be markedly down-regulated by bufalin plus gefitinib.
CONCLUSIONSCombination of bufalin and gefitinib potently inhibited the growth of H1975 cells, and induced cell apoptosis. The potential mechanism for anti-tumor might be involved in blocking EGFR-PI3k/Akt pathway.
