Selective accumulation and growth inhibition of hybrid liposomes to human hepatocellular carcinoma cells in relation to fluidity of plasma membranes

Komizu, Yuji; Ueoka, Hidetsugu; Ueoka, Ryuichi

doi:10.1016/j.bbrc.2011.12.134

Cited by 18 publications

(10 citation statements)

References 30 publications

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“…HL‐23 inhibited the growth of LM8 cells in a dose‐dependent manner with a 50% inhibitory concentration (IC 50 ) value of 205 μmol/L for DMPC, whereas DMPC liposomes slightly inhibited the growth of LM8 cells in the concentration range of 0–500 μmol/L for DMPC (IC 50 >500 μmol/L). In our previous study, it was reported that HL‐23 induced apoptotic cell death in various tumor cells including human OS (U‐2 OS, MG‐63) cells in vitro . Here, we observed the induction of apoptosis by HL‐23 in LM8 cells on the basis of Hoechst 33342 staining assay.…”

Section: Resultsmentioning

confidence: 55%

“…We have also demonstrated a good correlation between fluidity of plasma membranes of various cancer cells and anticancer effects of HL in vitro . Significantly, the HL distinguished cancer cells and normal cells which have higher and lower membrane fluidities, respectively, and fused and accumulated preferentially into cancer cells for human hepatocarcinoma and human adult T‐cell leukemia cells . Recently, we have reported the inhibitory effects of HL‐23 on the growth and invasion/migration of human OS (U‐2 OS) cells along with apoptosis in vitro .…”

Section: Introductionmentioning

confidence: 68%

“…HL‐23, being more fluid as compared with DMPC liposomes, showed strong inhibitory effects on the growth of U‐2 OS and MG‐63 cells and human colon tumor (WiDr) cells . The high inhibitory effects of HL‐23 on the growth of LM8 cells should be closely related to the membrane fluidity of HL‐23, probably due to the membrane fusion of HL‐23 with the tumor cells . Plausibly, HL‐23 could fuse and accumulate into LM8 cell membranes, and inhibit the growth of LM8 cells through the induction of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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Hybrid liposomes inhibit tumor growth and lung metastasis of murine osteosarcoma cells

et al. 2013

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Antitumor effects of hybrid liposomes (HL) composed of l-α-dimyristoylphosphatidylcholine (DMPC) and polyoxyethylene(23) dodecyl ether (C12(EO)23) on the metastatic growth of murine osteosarcoma (LM8) cells were investigated in vitro and in vivo. Remarkable inhibitory effects of HL-23 on the growth of LM8 cells were obtained through the induction of apoptotic cell death in vitro. It was also indicated that HL-23 should dramatically suppress the invasion of LM8 cells and the formation of filopodia on the cell surface in vitro. Furthermore, significantly high therapeutic effects were observed in the homograft mouse models of LM8 cells with lung metastasis after the treatment with HL-23 in vivo. That is, the histological analysis demonstrated that the primary tumor growth of LM8 cells implanted subcutaneously into the mice was inhibited along with the induction of apoptosis. In addition, it was found that HL-23 significantly decreased the lung metastasis of LM8 cells in the mouse models through the inhibition of primary tumor invasion. These results suggest that HL-23 could be a novel agent for the chemotherapy of osteosarcoma.

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Section: Resultsmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

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Hybrid liposomes inhibit tumor growth and lung metastasis of murine osteosarcoma cells

et al. 2013

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“…HL/ICG did not accumulate in normal colon cells. The membrane fluidity of tumor cells is considered to be higher than that of normal cells (Papahadjopoulos et al., 1973 ; Deliconstantinos, 1987 ; Sok et al., 1999 ; Komizu et al., 2011 ; Komizu et al., 2012 ). These results suggest that there is selective accumulation (useful for diagnosis) of HL/ICG only in colorectal cancer cells that have a greater degree of membrane fluidity compared to normal colon cells.…”

Section: Resultsmentioning

confidence: 99%

Hybrid liposomes showing enhanced accumulation in tumors as theranostic agents in the orthotopic graft model mouse of colorectal cancer

2018

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Hybrid liposomes (HLs) can be prepared by simply sonicating a mixture of vesicular and micellar molecules in a buffer solution. This study aimed to elucidate the therapeutic effects and ability of HLs to detect (diagnosis) cancer in an orthotopic graft mouse model of colorectal cancer with HCT116 cells for the use of HLs as theranostic agents. In the absence of a chemotherapeutic drug, HLs exhibited therapeutic effects by inhibiting the growth of HCT116 colorectal cancer cells in vitro, possibly through an increase in apoptosis. Intravenously administered HLs also caused a remarkable reduction in the relative cecum weight in an orthotopic graft mouse model of colorectal cancer. A decrease in tumor size in the cecal sections was confirmed by histological analysis using HE staining. TUNEL staining indicated an induction of apoptosis in HCT116 cells in the orthotopic graft mouse model of colorectal cancer. For the detection (diagnosis) of colorectal cancer by HLs, the accumulation of HLs encapsulating a fluorescent probe (ICG) was observed in HCT116 cells in the in vivo colorectal cancer model following intravenous administration. These data indicate that HLs can accumulate in tumor cells in the cecum of the orthotopic graft mouse model of colorectal cancer for a prolonged period of time, and inhibit the growth of HCT116 cells.

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“…HL, composed of L-α-dimyristoylphosphatidylcholine (DMPC) and polyoxyethylene (23) dodecyl ethers (C 12 (EO) 23 ), are effective for inhibiting the growth of various cancer cells in vitro [6][7][8][9], in vivo [10,11] and clinical applications [12]. Recently, we have reported that HL composed of 90 mol% DMPC and 10 mol% C 12 (EO) 23 induced apoptosis in various cancer cells including NSCLC (A549, H460, H23 and H520) cells [9,[13][14][15]. Furthermore, HL-induced apoptosis in A549 cells was caused by the activation of caspases-3, -8, -9 and the reduction of mitochondrial membrane potential [15].…”

Section: Introductionmentioning

confidence: 99%

Cell Cycle Arrest by Hybrid Liposomes for Human Lung Carcinoma Cells

Komizu¹,

Yukihara²,

Matsumoto

et al. 2014

J Carcinog Mutagen

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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 G 0 /G 1 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 p21 WAF1/CIP1 and p27 KIP1 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 G 0 /G 1 phase could be associated by the up-regulation of cdk inhibitor p21 and p27 through blocking Akt signaling.

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Selective accumulation and growth inhibition of hybrid liposomes to human hepatocellular carcinoma cells in relation to fluidity of plasma membranes

Cited by 18 publications

References 30 publications

Hybrid liposomes inhibit tumor growth and lung metastasis of murine osteosarcoma cells

Hybrid liposomes inhibit tumor growth and lung metastasis of murine osteosarcoma cells

Hybrid liposomes showing enhanced accumulation in tumors as theranostic agents in the orthotopic graft model mouse of colorectal cancer

Cell Cycle Arrest by Hybrid Liposomes for Human Lung Carcinoma Cells

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