Inhibitory effect of 17AAG-cypate polymer micelles on A549 cell xenografts in nude mice in vivo
10.3760/cma.j.issn.1004-4221.2019.12.011
- VernacularTitle: 17AAG-Cypate聚合物胶束对A549细胞裸鼠移植瘤抑瘤效果的体内实验研究
- Author:
Yiru PENG
1
;
Chenglong CHEN
2
;
Nan ZHANG
1
;
Lian XUE
2
;
Dong YU
1
Author Information
1. School of Radiation Medicine and Protection, Soochow University, Suzhou 215000, China
2. School of Public Health Medical, Soochow University, Suzhou 215000, China
- Publication Type:Journal Article
- Keywords:
17AAG-cypate micelles;
Tumor graft;
A549 cell line;
Nude mouse
- From:
Chinese Journal of Radiation Oncology
2019;28(12):928-932
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the inhibitory effect of 17AAG-Cypate micelles on the non-small cell lung cancer A549 cells in nude mice and to explore its possible mechanism.
Methods:A549 lung adenocarcinoma tumor-bearing nude mice were established. The nude mice were treated with saline ( saline group), X-ray (X-ray group), 17AAG micelles+ X-ray (17AAG-M/X group) and 17AAG-Cypate micelles+ laser/X-ray (17AAG-Cypate-M/L+ X group), respectively. The growth of xenograft tumors in different groups was measured on a regular basis to delineate the growth curve. The expression of proliferating cell nuclear antigen (PCNA) was measured by immunohistochemistry. The microvascular density was detected. The apoptosis of xenograft tissues was observed by TUNEL staining. The expression levels of p-ERK1/2 and p-AKT were quantitatively measured by Western blot.
Results:Compared with the saline group, varying degrees of inhibition of tumor growth were observed in the X-ray, 17AAG-M/X-ray and 17AAG-Cypate-M/L+ X groups, particularly in the 17AAG-Cypate-M/L+ X group (all P<0.05). In all groups, the expression levels of PCNA were significantly down-regulated (all P<0.05), the microvascular density was remarkably reduced (all P<0.05) and the expression levels of p-ERK1/2 and p-AKT were considerably down-regulated (all P<0.05).
Conclusions:17AAG-Cypate micelles can inhibit the growth of human non-small cell lung cancer in nude mice, probably by reducing the activity of p-ERK1/2 and p-AKT, thereby weakening the activation of the MAPK-ERK and PI3K-AKT signaling pathways.
