alexa Cell Cycle Arrest by Hybrid Liposomes for Human Lung Carcinoma Cells | OMICS International | Abstract
ISSN: 2157-2518

Journal of Carcinogenesis & Mutagenesis
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Research Article

Cell Cycle Arrest by Hybrid Liposomes for Human Lung Carcinoma Cells

Yuji Komizu, Mamiko Yukihara, Yoko Matsumoto* and Ryuichi Ueoka

Division of Applied Life Science, Graduate School of Engineering, Sojo University, Japan

*Corresponding Author:
Yoko Matsumoto
Division of Applied Life Science, Graduate School of Engineering
Sojo University, 4-22-1 Ikeda, Nishi-ku, Kumamoto 860-0082, Japan
Tel: +81-96-326-3956
Fax: +81-96-326-0522
E-mail: [email protected]

Received date: December 12, 2013; Accepted date: January 15, 2014; Published date: January 21, 2014

Citation: Komizu Y, Yukihara M, Matsumoto Y, Ueoka R (2014) Cell Cycle Arrest by Hybrid Liposomes for Human Lung Carcinoma Cells. J Carcinog Mutagen 5:157. doi: 10.4172/2157-2518.1000157

Copyright: © 2014 Komizu Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Hybrid liposomes (HL), composed of L-α-dimyristoylphosphatidylcholine and polyoxyethylene(23) dodecyl ethers, were simply prepared by the sonication method. In this study, we investigated the effects of HL on cell cycle and apoptosis in human non-small cell lung cancer cells. Induction of cell cycle arrest at the G0/G1 phase and apoptosis by HL were observed in human non-small cell lung cancer cells (A549, H460 and H23). HL treatment also resulted in the induction of cyclin-dependent kinases inhibitor p21WAF1/CIP1 and p27KIP1 and a decrease in the protein expressions of cyclins D1 and E. It is noteworthy that the treatment of A549 cells with HL inhibited phosphorylation of Akt in a time- and dose-dependent manner. Furthermore, HL treatment inhibited the filopodia formation in A549 cells. These results suggest that HL-induced cell cycle arrest at the G0/G1 phase could be associated by the up-regulation of cdk inhibitor p21 and p27 through blocking Akt signaling

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