發明
中華民國
103146429
I 521207
大腸癌之檢測方法及其應用
高雄醫學大學
2016/02/11
腫瘤的微環境對於癌症的發展過程中是一個很重要的決定因子。在本次的研究中主要是去探討腫瘤相關樹突細胞所分泌的過敏細胞激素會促進大腸癌細胞的遷移、入侵及上皮細胞轉型成間質細胞的過程。本實驗利用重組會大量表現在大腸癌腫瘤相關樹突細胞周圍的人類化學激素(C-C 基序)受質5 (CCL5),去模仿在腫瘤相關樹突細胞環境的培養基所促進大腸癌細胞的遷移、入侵及上皮細胞轉型成間質細胞的過程。 利用中和抗體去阻斷CCL5可以降低腫瘤相關樹突細胞所促進癌細胞的發展。另外在人類大腸癌切片發現腫瘤浸潤的CD11c+樹突細胞會分泌出CCL5。我們的研究結果顯示出去抑制CCL5或CCL5相關的訊息傳遞可能會成為一個新的大腸癌病患的治療標靶。 The tumor microenvironment is a critical factor determining the development of cancer. The aim of this study was to investigate the inflammatory cytokines secreted by tumor-associated dendritic cells (TADCs) that contribute to enhanced migration, invasion and epithelial-to-mesenchymal transition (EMT) in colon cancer. The administration of recombinant human chemokine (C-C motif) ligand 5 (CCL5), which is large expressed by colon cancer surrounding TADCs, mimicked stimulation of TADC-conditioned medium on the migration, invasion, and EMT in colon cancer cells. Blockade of CCL5 by neutralizing antibodies diminished the promotion of cancer progression by TADCs. The production of CCL5 was found in tumor-infiltrating CD11c+ DCs in human colon cancer specimens. Our findings suggest that inhibition of CCL5 or CCL5-related signaling may be an attractive therapeutic target in colon cancer patients.
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