癌症在全球是導致人們死亡的重要疾病之一。在整個病程中，癌症轉移導致了90%癌症病患的死亡，癌細胞從原發腫瘤入侵血管後藉由體內的血液循環系統轉移至其它器官或身體部位，在癌症轉移的進展中，循環腫瘤細胞簇（Circulating tumor microemboli, CTM）起著至關重要的作用，通過血管或微血管中的滾動黏附(rolling-adhesion)或物理閉塞(physical occlusion)來造成癌細胞外滲(extravasation)達到癌症二次轉移，形成繼發性腫瘤。雖然 CTM 很少發生，但其高轉移潛力與疾病的進展相關。在此研究中，我們建立一個微流體漸縮血管模型對CTM遭遇物理閉塞之轉移現象進行模擬。首先，我們透過探針預放入於微流體通道，內涵未聚合的纖維蛋白與膠原蛋白水凝膠，在等待其固化後產生直徑由600 µm漸縮最小至70 µm的錐形通道，爾後在管腔內側接種人類臍靜脈內皮細胞(Human Umbilical Vein Endothelial Cells, HUVECs)形成一漸縮血管之結構。藉由加入螢光標記物(分子量70kDa之FITC-dextran)比較漸縮血管與中空結構的通透性，結果顯示漸縮血管具有滲透性為5.5 x 10-7 cm/s之良好的屏障功能。通過培養乳癌腫瘤球體建立CTM模型並將其放入由血管內皮所形成的錐形漸縮血管中觀察細胞球在不同位置上所表現的行為。研究結果顯示，細胞球在越小的管徑中，可以引發癌細胞產生ㄧ較多絲狀偽足（filopodia）之結構與較侵襲之現象。本研究建構之微流體漸縮血管模型預期可以為癌細胞於轉移時所遭遇之物理閉塞過程提供更進一步的了解。

Cancer is one of the most lethal diseases, causing millions of deaths worldwide. Cancer metastasis is the cause of death in 90% of cancer patients. Circulating tumor microemboli (CTMs) in cancer metastasis are believed to play a vital role in the progression of cancer metastasis. The mechanisms of CTM extravasation are believed to be dependent on rolling adhesion and physical occlusion in blood vessels or capillaries. Although CTMs rarely occur, studies have shown that their high metastatic potential is related to disease progression. In this study, a microfluidic vessel-on-a-chip model was established to simulate the mode of CTM migration in a blood vessel. In this thesis, we placed the probe needle in a microfluidic channel containing unpolymerized hydrogel (fibrin/collagen type I) in advance and waited for polymerization. This method can form a tapered channel with a diameter varying from 600 µm to a minimum of 70 µm, and human umbilical vein endothelial cells (HUVECs) can be loaded into the lumen to form an in vitro tapered vascular model. Adding a fluorescent marker (FITC-dextran with a molecular weight of 70 kDa) to compare the permeability of the tapered vessel and the empty lumen showed that the tapered vessel performs a good barrier function with the permeability at 5.5 x 10-7 cm/s. The CTM was established by culturing breast tumor spheroids and placing them in the tapered blood vessel formed by vascular endothelium to observe the behavior of the spheroids at different positions. The results of the study show that the smaller the diameter of the cell spheroid is, the more aggressive the cancer cells are with pronounced filopodia formation. This microfluidic vessel-on-a-chip model is believed to provide insights in the role of occluded CTM in potentiating the process of cancer metastasis.

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