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Over-expression of adenine nucleotide translocase 1 (ANT1) induces apoptosis and tumor regression in vivo

Cited 29 time in Web of Science Cited 34 time in Scopus
Authors
Jang, Ji-Young; Choi, Yun; Jeon, Yoon-Kyung; Aung, Khin Chaw Yu; Kim, Chul-Woo
Issue Date
2008-06-04
Publisher
BioMed Central
Citation
BMC Cancer 2008, 8:160
Abstract
Background: Adenine nucleotide translocase (ANT) is located in the inner mitochondrial membrane and catalyzes the exchange of mitochondrial ATP for cytosolic ADP. ANT has been known to be a major component of the permeability transition pore complex of mitochondria and contributes to mitochondria-mediated apoptosis. Human ANT has four isoforms (ANT1, ANT2, ANT3, and ANT4), and the expression of the ANT isoforms is variable depending on the tissue and cell type, developmental stage, and proliferation status. Among the isoforms, ANT1 is highly expressed in terminally-differentiated tissues, but expressed in low levels in proliferating cells, such as cancer cells. In particular, over-expression of ANT1 induces apoptosis in cultured tumor cells.
Methods: We applied an ANT1 gene transfer approach to induce apoptosis and to evaluate the anti-tumor effect of ANT1 in a nude mouse model.
Results: We demonstrated that ANT1 transfection induced apoptosis of MDA-MB-231 cells, inactivated NF-κB activity, and increased Bax expression. ANT1-inducing apoptosis was accompanied by the disruption of mitochondrial membrane potential, cytochrome c release and the activation of caspases-9 and -3. Moreover, ANT1 transfection significantly suppressed tumor growth in vivo.
Conclusion: Our results suggest that ANT1 transfection may be a useful therapeutic modality for the treatment of cancer.
ISSN
1471-2407
Language
English
URI
http://www.biomedcentral.com/1471-2407/8/160

http://hdl.handle.net/10371/3856
DOI
https://doi.org/10.1186/1471-2407-8-160

https://doi.org/10.1186/1471-2407-8-160
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College of Medicine/School of Medicine (의과대학/대학원)Pathology (병리학전공)Journal Papers (저널논문_병리학전공)
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