The attenuation of experimental lung metastasis by a bile acid acylated-heparin derivative

Kyeongsoon Park; Seok Ki Lee; Dai Hyun Son; Soo Ah Park; Kwangmeyung Kim; Hyo Won Chang; Eun jeong Jeong; Rang Woon Park; In San Kim; Ick Chan Kwon; Youngro Byun; Sang Yoon Kim

doi:10.1016/j.biomaterials.2007.02.001

The attenuation of experimental lung metastasis by a bile acid acylated-heparin derivative

Kyeongsoon Park, Seok Ki Lee, Dai Hyun Son, Soo Ah Park, Kwangmeyung Kim, Hyo Won Chang, Eun jeong Jeong, Rang Woon Park, In San Kim, Ick Chan Kwon, Youngro Byun, Sang Yoon Kim

Department of Pharmaceutical Sciences

Research output: Contribution to journal › Article › peer-review

39 Scopus citations

Abstract

The inhibitory efficacies of new bile acid acylated-heparin derivative (heparin-DOCA) were evaluated on experimental lung metastasis. We evaluated the effect of heparin-DOCA on intercellular interactions including those between B16F10 and thrombin-activated platelets and TNF-α-activated HUVECs, and between B16F10 and immobilized mouse P-selectin. In addition, the inhibitory effects of heparin-DOCA on adhesion and invasion of B16F10 to Matrigel were studied. In an animal mouse study, the blood clot formation and the retention of red fluorescence protein (RFP)-B16F10 in lungs were assessed after heparin-DOCA and RFP-B16F10 intravenous administration. Furthermore, we investigated the anti-metastatic effect of heparin-DOCA against lung metastasis induced by B16F10 and SCC7. Heparin-DOCA inhibited intercellular interactions between B16F10 and activated platelets or activated HUVECs by blocking P- and E-selectin-mediated interactions. Moreover, it reduced adhesion and invasion of B16F10 to ECM, thereby affecting the reduction of early retention of B16F10 in the lung. Heparin-DOCA attenuated lung colony formation on the surfaces and in interior of the lung, and attenuated metastasis by B16F10 and SCC7. These results suggest that heparin-DOCA may have potentials as therapeutic agent that prevents tumor metastasis and progression.

Original language	English
Pages (from-to)	2667-2676
Number of pages	10
Journal	Biomaterials
Volume	28
Issue number	16
DOIs	https://doi.org/10.1016/j.biomaterials.2007.02.001
State	Published - Jun 2007

Bibliographical note

Funding Information:
This work was supported by the Next Generation New Technology Development Program of the Korean Ministry of Commerce, Industry, and Energy (Grant no. # 10011353), Asan Institute for Life Science (2002-073) and the Ministry of Science and Technology F104AA010009-06A0101-00910 in Korea.

Keywords

Adhesion
B16F10 melanoma
Bile acid acylated-heparin derivative
Invasion
Lung metastasis

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10.1016/j.biomaterials.2007.02.001

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title = "The attenuation of experimental lung metastasis by a bile acid acylated-heparin derivative",

abstract = "The inhibitory efficacies of new bile acid acylated-heparin derivative (heparin-DOCA) were evaluated on experimental lung metastasis. We evaluated the effect of heparin-DOCA on intercellular interactions including those between B16F10 and thrombin-activated platelets and TNF-α-activated HUVECs, and between B16F10 and immobilized mouse P-selectin. In addition, the inhibitory effects of heparin-DOCA on adhesion and invasion of B16F10 to Matrigel were studied. In an animal mouse study, the blood clot formation and the retention of red fluorescence protein (RFP)-B16F10 in lungs were assessed after heparin-DOCA and RFP-B16F10 intravenous administration. Furthermore, we investigated the anti-metastatic effect of heparin-DOCA against lung metastasis induced by B16F10 and SCC7. Heparin-DOCA inhibited intercellular interactions between B16F10 and activated platelets or activated HUVECs by blocking P- and E-selectin-mediated interactions. Moreover, it reduced adhesion and invasion of B16F10 to ECM, thereby affecting the reduction of early retention of B16F10 in the lung. Heparin-DOCA attenuated lung colony formation on the surfaces and in interior of the lung, and attenuated metastasis by B16F10 and SCC7. These results suggest that heparin-DOCA may have potentials as therapeutic agent that prevents tumor metastasis and progression.",

keywords = "Adhesion, B16F10 melanoma, Bile acid acylated-heparin derivative, Invasion, Lung metastasis",

author = "Kyeongsoon Park and {Ki Lee}, Seok and {Hyun Son}, Dai and {Ah Park}, Soo and Kwangmeyung Kim and {Won Chang}, Hyo and Jeong, {Eun jeong} and Park, {Rang Woon} and Kim, {In San} and {Chan Kwon}, Ick and Youngro Byun and Kim, {Sang Yoon}",

note = "Funding Information: This work was supported by the Next Generation New Technology Development Program of the Korean Ministry of Commerce, Industry, and Energy (Grant no. # 10011353), Asan Institute for Life Science (2002-073) and the Ministry of Science and Technology F104AA010009-06A0101-00910 in Korea.",

year = "2007",

month = jun,

doi = "10.1016/j.biomaterials.2007.02.001",

language = "English",

volume = "28",

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AU - Park, Kyeongsoon

AU - Ki Lee, Seok

AU - Hyun Son, Dai

AU - Ah Park, Soo

AU - Kim, Kwangmeyung

AU - Won Chang, Hyo

AU - Jeong, Eun jeong

AU - Park, Rang Woon

AU - Kim, In San

AU - Chan Kwon, Ick

AU - Byun, Youngro

AU - Kim, Sang Yoon

N1 - Funding Information: This work was supported by the Next Generation New Technology Development Program of the Korean Ministry of Commerce, Industry, and Energy (Grant no. # 10011353), Asan Institute for Life Science (2002-073) and the Ministry of Science and Technology F104AA010009-06A0101-00910 in Korea.

PY - 2007/6

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N2 - The inhibitory efficacies of new bile acid acylated-heparin derivative (heparin-DOCA) were evaluated on experimental lung metastasis. We evaluated the effect of heparin-DOCA on intercellular interactions including those between B16F10 and thrombin-activated platelets and TNF-α-activated HUVECs, and between B16F10 and immobilized mouse P-selectin. In addition, the inhibitory effects of heparin-DOCA on adhesion and invasion of B16F10 to Matrigel were studied. In an animal mouse study, the blood clot formation and the retention of red fluorescence protein (RFP)-B16F10 in lungs were assessed after heparin-DOCA and RFP-B16F10 intravenous administration. Furthermore, we investigated the anti-metastatic effect of heparin-DOCA against lung metastasis induced by B16F10 and SCC7. Heparin-DOCA inhibited intercellular interactions between B16F10 and activated platelets or activated HUVECs by blocking P- and E-selectin-mediated interactions. Moreover, it reduced adhesion and invasion of B16F10 to ECM, thereby affecting the reduction of early retention of B16F10 in the lung. Heparin-DOCA attenuated lung colony formation on the surfaces and in interior of the lung, and attenuated metastasis by B16F10 and SCC7. These results suggest that heparin-DOCA may have potentials as therapeutic agent that prevents tumor metastasis and progression.

AB - The inhibitory efficacies of new bile acid acylated-heparin derivative (heparin-DOCA) were evaluated on experimental lung metastasis. We evaluated the effect of heparin-DOCA on intercellular interactions including those between B16F10 and thrombin-activated platelets and TNF-α-activated HUVECs, and between B16F10 and immobilized mouse P-selectin. In addition, the inhibitory effects of heparin-DOCA on adhesion and invasion of B16F10 to Matrigel were studied. In an animal mouse study, the blood clot formation and the retention of red fluorescence protein (RFP)-B16F10 in lungs were assessed after heparin-DOCA and RFP-B16F10 intravenous administration. Furthermore, we investigated the anti-metastatic effect of heparin-DOCA against lung metastasis induced by B16F10 and SCC7. Heparin-DOCA inhibited intercellular interactions between B16F10 and activated platelets or activated HUVECs by blocking P- and E-selectin-mediated interactions. Moreover, it reduced adhesion and invasion of B16F10 to ECM, thereby affecting the reduction of early retention of B16F10 in the lung. Heparin-DOCA attenuated lung colony formation on the surfaces and in interior of the lung, and attenuated metastasis by B16F10 and SCC7. These results suggest that heparin-DOCA may have potentials as therapeutic agent that prevents tumor metastasis and progression.

KW - Adhesion

KW - B16F10 melanoma

KW - Bile acid acylated-heparin derivative

KW - Invasion

KW - Lung metastasis

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DO - 10.1016/j.biomaterials.2007.02.001

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C2 - 17335894

AN - SCOPUS:33847656686

SN - 0142-9612

VL - 28

SP - 2667

EP - 2676

JO - Biomaterials

JF - Biomaterials

IS - 16

ER -

The attenuation of experimental lung metastasis by a bile acid acylated-heparin derivative

Abstract

Bibliographical note

Keywords

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