研究CCL3在人類軟骨肉瘤移行所扮演的角色

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题名:	研究CCL3在人類軟骨肉瘤移行所扮演的角色 Study the role of CCL3 in migration in human chondrosarcoma cells
作者:	陳清元;Chin-Yuan Chen
贡献者:	基礎醫學研究所碩士班
关键词:	CCL3;人類軟骨肉瘤;移行;CCL3;human chondrosarcoma;migration
日期:	2013-02-05
上传时间:	2013-10-02 11:16:43 (UTC+8)
出版者:	中國醫藥大學
摘要:	CCL3是CCL family (chemokine (C-C motif) ligand family) 中的一員，又稱為MIP-1α (macrophage inflammatory protein-1α)。是一種細胞因子，在細胞中參與發炎反應、多形核白血球的活化，也活躍於腫瘤細胞。軟骨肉瘤是一種高度惡性的腫瘤，且具有轉移性。基質金屬蛋白酶（matrix metalloproteinase）對細胞的行為，如細胞增殖，遷移，分化和血管生成中都發揮了重要作用。然而CCL3與軟骨肉瘤的移行關係並不明朗。本實驗中我們發現CCL3可以透過CCR5 receptor增加人類軟骨肉瘤細胞(JJ012&SW1353)的移行和MMP-2的表現。本實驗使用CCR5單株抗體可以有效地抑制CCL3誘導細胞移行能力和MMP-2的產生。給予CCL3後也會促進AMPK (AMP-activated protein kinase)、p38、IKKα/β及p65的活化；使用AMPK、 p38、IKKα/β和NF-κB (nuclear factor kappaB)專一性訊息傳遞抑制劑，都會抑制CCL3增加人類軟骨肉瘤細胞的移行能力與MMP-2的產生。細胞轉染AMPK siRNA、DN-p38、DN-IKKα/β、MMP-2 siRNA及CCL3 shRNA也可以有效降低CCL3促使癌症細胞的轉移。由我們的實驗結果指出CCL3會經過CCR5 receptor調控人類軟骨肉瘤細胞的移行能力與MMP-2的表現，而 AMPK / p38 / NF-κB 路徑參與其中。 Chemokine (C-C motif) ligand 3 (CCL3) is a protein that in humans is encoded by the CCL3 gene. CCL3, also known as Macrophage inflammatory protein-1α, is a cytokine involved in inflammation, activation of polymorphonuclear leukocytes and was detected in infiltrating cells and tumor cells. Chondrosarcoma is a type of highly malignant tumor and cause distant metastasis. Matrix metalloproteinases (MMPs) play a major role on cell behaviors such as cell proliferation, migration, differentiation and angiogenesis. However, the effects of CCL3 in migration and MMP-2 expression in chondrosarcoma cells are largely unknown. Here we found that CCL3 increased the migration and expression of MMP-2 in human chondrosarcoma cells (JJ012&SW1353 cells). Activations of CCR5, AMPK, p38, and nuclear factor-κB (NF-κB) pathways after CCL3 treatment were demonstrated, and CCL3-induced the expression of MMP-2 and migration activity was also inhibited by the specific inhibitor and dominant mutant of CCR5, AMPK, p38, and NF-κB cascades. Taken together, our result indicated that CCL3 enhances the cell migration ability of human chondrosarcoma cells by increasing MMP-2 expression via CCR5 receptor, AMPK, p38, and NF-κB pathway.
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