Novel mechanism of hybrid liposomes-induced apoptosis in human tumor cells
✍ Scribed by Yoko Matsumoto; Yasunori Iwamoto; Taku Matsushita; Ryuichi Ueoka
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- French
- Weight
- 542 KB
- Volume
- 115
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Hybrid liposomes can be prepared by simply ultrasonicating a mixture of vesicular and micellar molecules in a buffer solution. The physical properties of these liposomes, such as size, membrane fluidity, phase transition temperature and hydrophobicity can be controlled by changing the composition. Hybrid liposomes composed of dimyristoylphosphatidylcholine and polyoxyethylene (10) dodecyl ether were found to inhibit the growth of human promyelocytic leukemia (HL‐60) cells without using any drugs. Induction of apoptosis by hybrid liposomes in HL‐60 cells was verified on the basis of fluorescence microscopy and flow cytometry analysis, after fusion and accumulation of hybrid liposomes, which was revealed on the basis of microphysiometer. We elucidated the pathways of apoptosis induced by the hybrid liposomes. That is, hybrid liposomes fused and accumulated in tumor cell membranes, and the apoptosis signal first passed through mitochondria, caspase‐9 and caspase‐3, second through Fas, caspase‐8, caspase‐3 and then reached the nucleus. Hybrid liposomes themselves can induce apoptosis in human tumor cells along with high inhibitory effects on the growth of tumor cells. © 2005 Wiley‐Liss, Inc.
📜 SIMILAR VOLUMES
## Abstract Taxol is extensively used clinically for chemotherapy of patients with ovarian, breast, and lung cancer. Although taxol induces apoptosis of cancer cells, its exact mechanism of action is not yet known. To determine the mechanism of action of taxol in ovarian cancer, we tested the effec
## Abstract 2‐Methoxyestradiol, a well‐known nonpolar endogenous metabolite of 17β‐estradiol, has been shown to selectively induce apoptosis in a number of cancer cell lines, but not in normal cells. The mechanism of 2‐methoxyestradiol‐induced apoptosis appears to vary considerably in different cel