Effect of autophagy-related gene Beclin 1 on growth of xenografts of human lung adenocarcinoma A549 cells in nude mice / 肿瘤
Tumor
;
(12): 1061-1066, 2011.
Article
in Chinese
| WPRIM
| ID: wpr-849115
ABSTRACT
Objective:
To investigate the effect of autophagy-related gene Beclin 1 on growth of xenografts of human lung adenocarcinoma A549 cells in BALB/c nude mice.Methods:
The recombined plasmids pRNAT-U6.2/Lenti-si423 and pLenex-Beclin 1 were transiently transfected by lipofectin regeant into A549 cells, respectively. The expression levels of Beclin 1 mRNA and protein in A549 cells were detected by real-time fluorogenic quantitative-PCR (RFQ-PCR) and Western blotting, respectively. The proliferation rate of A549 cells transfected with recombinant vector pRNAT-U6.2/Lenti-si423 or pLenex-Beclin 1 was determined by MTT assay. The A549 cells expressing Beclin 1 or with Beclin 1 silencing were subcutaneously injected into right axillary region of nude mice. The growth rate and size of xenograft tumor were observed, and the expression levels of Beclin 1 mRNA and protein in xenograft tumor were determined by RFQ-PCR and immunohistochemistry, respectively.Results:
The expression levels of Beclin 1 mRNA and protein were increased in A549 cells transfected with recombinant vector pLenex-Beclin 1, and the cell proliferation in vitro was inhibited. The expression levels of Beclin 1 mRNA and protein were decreased in A549 cells transfected with recombinant vector pRNAT-U6.2/Lenti-si423. As compared with Beclin 1-silencing group, the growth rate of subcutaneous xenograft was slowing down with lower weight and smaller volume and the relative expression levels of Beclin 1 mRNA and protein were both higher in Beclin 1-overexpression group.Conclusion:
Autophagy-related gene Beclin 1 can inhibit the growth of xenograft of human lung adenocarcinoma A549 cells in nude mice, and it may become a new target for tumor therapy. Copyright© 2011 by TUMOR.
Full text:
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Index:
WPRIM (Western Pacific)
Language:
Chinese
Journal:
Tumor
Year:
2011
Type:
Article
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