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Over-expression of PTEN on proliferation and apoptosis in canine mammary tumors cells

Animal Cells and Systems 2016년 20권 6호 p.325 ~ 334
Tong Jinjin, Zhang Hua, Sun Dongdong, Wang Yingxue, Yang Chao, Liu Yun,
소속 상세정보
 ( Tong Jinjin ) - Northeast Agricultural University College of Veterinary Medicine Department of Veterinary Surgery
 ( Zhang Hua ) - Beijing University of Agriculture College of Animal Science and Technology
 ( Sun Dongdong ) - Northeast Agricultural University College of Veterinary Medicine Department of Veterinary Surgery
 ( Wang Yingxue ) - Northeast Agricultural University College of Veterinary Medicine Department of Veterinary Surgery
 ( Yang Chao ) - Northeast Agricultural University College of Veterinary Medicine Department of Veterinary Surgery
 ( Liu Yun ) - Northeast Agricultural University College of Veterinary Medicine Department of Veterinary Surgery

Abstract


Phosphatase and tensin homolog (PTEN) is an important tumor-suppressor gene which constitutes an important PI3K/Akt pathway by regulating the signaling of multiple biological processes, including apoptosis, metabolism, cell proliferation, and cell growth has been gaining increasing attention. However, the role of PTEN in regulating apoptosis of canine mammary tumors cells still needs further investigation. In this experiment, the effect of PTEN on proliferation and apoptosis in canine mammary tumors (CMT) cells was analyzed. As a result, gene and protein expression levels of apoptosis-related genes were detected. Eukaryotic expression vector pcDNA3.1+-PTEN were successfully constructed and stably transferred into canine CMT cells after geneticin (G418) selection. After pcDNA3.1+-PTEN transfection, compared with control group, the cells proliferation was inhibited and the cell apoptosis was increased in CMT cells. The expression of p-Akt was decreased and the apoptosis-related genes, such as caspase-3, caspase-9, and Bax, were increased. These data serve to demonstrate the function of PTEN on apoptosis and gene regulatory in PI3K/Akt pathway in CMT cells. Collectively, our data link the tumor-suppressor activities of PTEN to the machinery controlling cell cycle through the modulation of signaling molecules whose signal target is the functional inactivation of the apoptosis gene product.

키워드

Tumor suppressor; PI3K/Akt pathway; therapy

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