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

Highlights

  • Non-small cell lung carcinoma (NSCLC), including adenocarcinoma, squamous-cell lung carcinoma, and large-cell lung carcinoma, is the most common form of lung cancer and accounts for the most deaths of any cancer worldwide

  • We have reported that hybrid liposomes (HL) composed of 90 mol% DMPC and 10 mol% C12(EO)23 induced apoptosis in various cancer cells including NSCLC (A549, H460, H23 and H520) cells [9,13,14,15]

  • We investigated the effects of HL composed of 90 mol% DMPC and 10 mol% C12(EO)23 on the cell cycle and apoptosis of NSCLC (A549, H460 and H23) cells in vitro, and found the induction of cell cycle arrest at G0/G1 phase through blocking Akt signaling along with apoptosis

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Summary

Introduction

Non-small cell lung carcinoma (NSCLC), including adenocarcinoma, squamous-cell lung carcinoma, and large-cell lung carcinoma, is the most common form of lung cancer and accounts for the most deaths of any cancer worldwide. We have reported that HL composed of 90 mol% DMPC and 10 mol% C12(EO) induced apoptosis in various cancer cells including NSCLC (A549, H460, H23 and H520) cells [9,13,14,15]. We have reported that HL inhibits the growth of colorectal cancer (HCT116) cells through the induction of cell cycle arrest at G0/G1 phase along with apoptosis [16]. We investigated the effects of HL composed of 90 mol% DMPC and 10 mol% C12(EO) on the cell cycle and apoptosis of NSCLC (A549, H460 and H23) cells in vitro, and found the induction of cell cycle arrest at G0/G1 phase through blocking Akt signaling along with apoptosis

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