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Overexpression of beclin1 induced autophagy and apoptosis in lungs of K-ras(LA1) mice

Cited 21 time in Web of Science Cited 23 time in Scopus
Authors
Shin, Ji Young; Hong, Seong-Ho; Kang, Bitna; Minai-Tehrani, Arash; Cho, Myung-Haing
Issue Date
2013-09
Citation
Lung Cancer, Vol.81 No.3, pp.362-370
Keywords
Beclin1AutophagyApoptosisMitochondriaLung cancerGene therapy
Abstract
Beclin1, as a key molecule in controlling autophagy pathway, can activate both cell survival and cell death pathway. As a role of autophagy in cancer progression remains controversial, introduction of beclin1 to the lungs of K-ras(LA1) mice was performed via inhalation. Prolonged autophagy activation was induced by repeated exposure of lentivirus-beclin1, total of 8 times (2 times/week, 4 weeks). By the time of sacrifice, lungs were collected and analyzed for the therapeutic efficacy. Total numbers of tumors on the surface and histopathological tumor progression were reduced in the lungs of K-ras(LA1) mice. Successful delivery of beclin1 induced autophagy and apoptosis in the target organ, which were confirmed by following features; increased autophagic vacuoles in the cytosol, increased number of mitochondria with decreased mitochondrial 12S RNA, and increased protein levels of mitochondria-related apoptosis. Markers for cell proliferation and angiogenesis, PCNA and VEGF, which used for prediction of cancer prognosis, were significantly reduced after introduction of beclin1. Taken together, the results indicate that autophagy regulating gene, beclin1, can be a potential target for lung cancer gene therapy. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
ISSN
0169-5002
URI
https://hdl.handle.net/10371/172466
DOI
https://doi.org/10.1016/j.lungcan.2013.05.009
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College of Veterinary Medicine (수의과대학)Dept. of Veterinary Medicine (수의학과)Journal Papers (저널논문_수의학과)
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