Effect of adenovirus-mediated ING4 and IL-24 co-expression on chemosensitivity to human lung adenocarcinoma in vitro and in vivo.
- Author:
Yehan ZHU
1
;
Xianrong DU
;
Huaxin CHEN
;
Yufeng XIE
;
Weihua SHENG
;
Jicheng YANG
Author Information
1. Department of Respiratory, First Affiliated Hospital in Soochow University, Suzhou 215006, China. zhuyehansz@sina.com
- Publication Type:Journal Article
- MeSH:
Adenocarcinoma;
drug therapy;
metabolism;
Adenoviridae;
genetics;
metabolism;
Animals;
Antineoplastic Agents;
pharmacology;
Apoptosis;
Cell Cycle Proteins;
biosynthesis;
genetics;
Cell Line, Tumor;
Gene Expression Regulation, Neoplastic;
Genetic Vectors;
Homeodomain Proteins;
biosynthesis;
genetics;
Humans;
Interleukins;
biosynthesis;
genetics;
Lung Neoplasms;
drug therapy;
metabolism;
Mice;
Mice, Nude;
Neoplasms, Experimental;
drug therapy;
Recombinant Fusion Proteins;
biosynthesis;
genetics;
pharmacology;
Transfection;
Tumor Suppressor Proteins;
biosynthesis;
genetics
- From:
Chinese Journal of Biotechnology
2011;27(1):85-94
- CountryChina
- Language:Chinese
-
Abstract:
To study the chemosensitivity and the mechanisms of recombinant adenovirus vector expressing ING4 and IL-24 (Ad-ING4-IL-24) on lung adenocarcinoma in vitro and in vivo, the expression of ING4 and IL-24 in A549 cells was detected by RT-PCR and Western blotting. The growth inhibition, apoptosis rate and apoptosis body were measured by MTT, flow cytometry and Hoechst staining respectively. For in vivo study, we first established the A549 tumor model by grafting A549 cells in athymic nude mice; and then injected Ad-ING4-IL-24 into the tumors. Two weeks after injection, we killed the mice, removed the tumors, weighted and calculated the ratios of tumor-suppression. We also detected the expressions of ING4, IL-24, bax, bcl-2, VEGF with immunohistochemistry. The results indicated that ING4 and IL-24 were proved successfully transcription and expression in A549 cells. More interestingly, the joint group inhibited the growth of A549 cells and induced apoptosis. The in vivo data showed that the joint group suppressed the tumor growth conspicuously through up-regulating the expression of bax, and down-regulating the expression of bcl-2, VEGF. The study proved that Ad-ING4-IL-24 significantly enhanced the chemosensitivity to anticancer drug DDP in lung adenocarcinoma, which may related with cell apoptosis and antiangiogenesis.
