FasL 是一個廣為人知的穿膜蛋白，它最著名的功能是與Fas 結合進而引發細胞凋亡。之前的研究發現，腫瘤細胞表現FasL 可以引發淋巴細胞進行細胞凋亡進而促進腫瘤的轉移。為了進一步探討FasL 是否調控腫瘤細胞的移行與轉移，我們建立了兩個帶有FasL 基因缺失的質體，其中一個失去了FasL 細胞質端的CKI 結合區域，另一個則同時失去了CKI 結合區域以及proline‐rich 區域。我們先在NIH 3T3 細胞中過量表現完整的FasL或者細胞質端缺失的FasL，再衡量細胞在體外或體內實驗模式下移行的變化。我們發現不論是過量表現完整的FasL 或細胞質端缺失的FasL 都不會影響細胞的生長與細胞週期進程，而且在體外實驗模式中兩者都會促進細胞的移行和侵犯能力。此外，這個由FasL 引發的細胞移行並不是透過ERK 或者PI3 激酶的活性所達成。進一步發現，只有截去細胞質端的FasL 可以促進腫瘤細胞在體內實驗模式中的轉移能力，並且加強體外實驗中的細胞轉型能力，而完整的FasL 則不具有這些能力。我們的結論是，截去FasL 的細胞質端會促進腫瘤細胞的轉移和轉型能力。

FasL is a well known death‐inducing transmembrane protein which binds to Fas and induces cell apoptosis. It was thought that tumor FasL induces apoptosis in infiltrating lymphocytes which results in increased tumor metastasis. To investigate whether FasL regulates tumor cell migration and metastasis, we constructed two plasmids each containing FasL with deletion of various cytoplasmic domain. One of them was deleted at the CKI‐binding motif and the other one lost both CKI‐binding motif and proline‐rich domain of Fas ligand cytoplasmic domain. We overexpressed the full length FasL or the cytoplasmic domain‐truncated FasL in NIH 3T3 cells and measured the alterations of cell motility in vitro and tumor metastasis in vivo. Overexpression of FasL or truncated FasL enhanced cell migration and invasiveness in vitro. In addition, the FasL induced cell migration is independent of ERK and PI3 kinase activity. However, only the truncated Fas ligand, but not the full‐length FasL, promoted tumor metastasis in vivo and increased cell transformation in vitro. In conclusion, truncated cytoplasmic domain of FasL promoted tumor metastasis and transformation.

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