Galectin-1-Mediated tumor invasion and metastasis, Up-Regulated matrix metalloproteinase expression, and reorganized actin cytoskeletons

Ming Heng Wu, Tse-Ming Hong, Hui Wen Cheng, Szu Hua Pan, Yu Ray Liang, Hsiao Chin Hong, Wei Fan Chiang, Dung-Yau Wang, Dar-Bin Shieh, Ai-Li Shiau, Ying Tai Jin, Yuh-Ling Chen

研究成果: Article

104 引文 (Scopus)

摘要

Galectin-1 (Gal-1) is a β-galactose-binding lectin; its expression level has been reported to correlate with tumor progression, Gal-1 is highly expressed in the invasive front of primary tumors and in the cancer cells of metastatic lesions in the lymph nodes of patients with oral squamous cell carcinoma. However, the molecular mechanism of Gal-1 in tumor metastasis is not completely clear. We found that increased Gal-1 expression is closely associated with its high levels of invasion in lung adenocarcinoma and oral squamous cell carcinoma cell lines. Knocking down Gal-1 with small interfering RNA in highly invasive cancer ceils reduced their invasion levels. Moreover, the invasion ability of poorly invasive cancer cells was significantly increased after Gal-1 overexpression of Gal-1. Mechanism studies revealed that Gal-1 promoted tumor invasion mainly by up-regulating matrix metalloproteinase (MMP)-9 and MMP-2 and by reorganizing actin cytoskeleton. Gal-1 enhanced the activation of Cdc42, a small GTPase and member of the Rho family, thus increasing the number and length of filopodia on tumor cells. Furthermore, Gal-1 -overexpressing cells had higher metastatic abilities in tail vein metastasis assays in vivo. We conclude that Gal-1 is involved in tumor invasion and metastasis by increasing MMP expression and reorganizing cytoskeletons in oral cancers and lung adenocarcinoma.

原文English
頁(從 - 到)311-318
頁數8
期刊Molecular Cancer Research
7
發行號3
DOIs
出版狀態Published - 2009 三月 1

指紋

Galectin 1
Matrix Metalloproteinases
Actin Cytoskeleton
Neoplasm Metastasis
Neoplasms
Aptitude
Squamous Cell Carcinoma
Galectins
Pseudopodia
Monomeric GTP-Binding Proteins
Mouth Neoplasms
Matrix Metalloproteinase 2
Matrix Metalloproteinase 9
Cytoskeleton
Small Interfering RNA
Veins
Lung Neoplasms

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Oncology
  • Cancer Research

引用此文

Wu, Ming Heng ; Hong, Tse-Ming ; Cheng, Hui Wen ; Pan, Szu Hua ; Liang, Yu Ray ; Hong, Hsiao Chin ; Chiang, Wei Fan ; Wang, Dung-Yau ; Shieh, Dar-Bin ; Shiau, Ai-Li ; Jin, Ying Tai ; Chen, Yuh-Ling. / Galectin-1-Mediated tumor invasion and metastasis, Up-Regulated matrix metalloproteinase expression, and reorganized actin cytoskeletons. 於: Molecular Cancer Research. 2009 ; 卷 7, 編號 3. 頁 311-318.
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abstract = "Galectin-1 (Gal-1) is a β-galactose-binding lectin; its expression level has been reported to correlate with tumor progression, Gal-1 is highly expressed in the invasive front of primary tumors and in the cancer cells of metastatic lesions in the lymph nodes of patients with oral squamous cell carcinoma. However, the molecular mechanism of Gal-1 in tumor metastasis is not completely clear. We found that increased Gal-1 expression is closely associated with its high levels of invasion in lung adenocarcinoma and oral squamous cell carcinoma cell lines. Knocking down Gal-1 with small interfering RNA in highly invasive cancer ceils reduced their invasion levels. Moreover, the invasion ability of poorly invasive cancer cells was significantly increased after Gal-1 overexpression of Gal-1. Mechanism studies revealed that Gal-1 promoted tumor invasion mainly by up-regulating matrix metalloproteinase (MMP)-9 and MMP-2 and by reorganizing actin cytoskeleton. Gal-1 enhanced the activation of Cdc42, a small GTPase and member of the Rho family, thus increasing the number and length of filopodia on tumor cells. Furthermore, Gal-1 -overexpressing cells had higher metastatic abilities in tail vein metastasis assays in vivo. We conclude that Gal-1 is involved in tumor invasion and metastasis by increasing MMP expression and reorganizing cytoskeletons in oral cancers and lung adenocarcinoma.",
author = "Wu, {Ming Heng} and Tse-Ming Hong and Cheng, {Hui Wen} and Pan, {Szu Hua} and Liang, {Yu Ray} and Hong, {Hsiao Chin} and Chiang, {Wei Fan} and Dung-Yau Wang and Dar-Bin Shieh and Ai-Li Shiau and Jin, {Ying Tai} and Yuh-Ling Chen",
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Galectin-1-Mediated tumor invasion and metastasis, Up-Regulated matrix metalloproteinase expression, and reorganized actin cytoskeletons. / Wu, Ming Heng; Hong, Tse-Ming; Cheng, Hui Wen; Pan, Szu Hua; Liang, Yu Ray; Hong, Hsiao Chin; Chiang, Wei Fan; Wang, Dung-Yau; Shieh, Dar-Bin; Shiau, Ai-Li; Jin, Ying Tai; Chen, Yuh-Ling.

於: Molecular Cancer Research, 卷 7, 編號 3, 01.03.2009, p. 311-318.

研究成果: Article

TY - JOUR

T1 - Galectin-1-Mediated tumor invasion and metastasis, Up-Regulated matrix metalloproteinase expression, and reorganized actin cytoskeletons

AU - Wu, Ming Heng

AU - Hong, Tse-Ming

AU - Cheng, Hui Wen

AU - Pan, Szu Hua

AU - Liang, Yu Ray

AU - Hong, Hsiao Chin

AU - Chiang, Wei Fan

AU - Wang, Dung-Yau

AU - Shieh, Dar-Bin

AU - Shiau, Ai-Li

AU - Jin, Ying Tai

AU - Chen, Yuh-Ling

PY - 2009/3/1

Y1 - 2009/3/1

N2 - Galectin-1 (Gal-1) is a β-galactose-binding lectin; its expression level has been reported to correlate with tumor progression, Gal-1 is highly expressed in the invasive front of primary tumors and in the cancer cells of metastatic lesions in the lymph nodes of patients with oral squamous cell carcinoma. However, the molecular mechanism of Gal-1 in tumor metastasis is not completely clear. We found that increased Gal-1 expression is closely associated with its high levels of invasion in lung adenocarcinoma and oral squamous cell carcinoma cell lines. Knocking down Gal-1 with small interfering RNA in highly invasive cancer ceils reduced their invasion levels. Moreover, the invasion ability of poorly invasive cancer cells was significantly increased after Gal-1 overexpression of Gal-1. Mechanism studies revealed that Gal-1 promoted tumor invasion mainly by up-regulating matrix metalloproteinase (MMP)-9 and MMP-2 and by reorganizing actin cytoskeleton. Gal-1 enhanced the activation of Cdc42, a small GTPase and member of the Rho family, thus increasing the number and length of filopodia on tumor cells. Furthermore, Gal-1 -overexpressing cells had higher metastatic abilities in tail vein metastasis assays in vivo. We conclude that Gal-1 is involved in tumor invasion and metastasis by increasing MMP expression and reorganizing cytoskeletons in oral cancers and lung adenocarcinoma.

AB - Galectin-1 (Gal-1) is a β-galactose-binding lectin; its expression level has been reported to correlate with tumor progression, Gal-1 is highly expressed in the invasive front of primary tumors and in the cancer cells of metastatic lesions in the lymph nodes of patients with oral squamous cell carcinoma. However, the molecular mechanism of Gal-1 in tumor metastasis is not completely clear. We found that increased Gal-1 expression is closely associated with its high levels of invasion in lung adenocarcinoma and oral squamous cell carcinoma cell lines. Knocking down Gal-1 with small interfering RNA in highly invasive cancer ceils reduced their invasion levels. Moreover, the invasion ability of poorly invasive cancer cells was significantly increased after Gal-1 overexpression of Gal-1. Mechanism studies revealed that Gal-1 promoted tumor invasion mainly by up-regulating matrix metalloproteinase (MMP)-9 and MMP-2 and by reorganizing actin cytoskeleton. Gal-1 enhanced the activation of Cdc42, a small GTPase and member of the Rho family, thus increasing the number and length of filopodia on tumor cells. Furthermore, Gal-1 -overexpressing cells had higher metastatic abilities in tail vein metastasis assays in vivo. We conclude that Gal-1 is involved in tumor invasion and metastasis by increasing MMP expression and reorganizing cytoskeletons in oral cancers and lung adenocarcinoma.

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