胰腺癌（Pancreatic cancer）大多發生在已開發的國家，2012年全球胰腺癌死亡率名列所有癌症的第七名，五年後的存活率僅有5%。這麼高的死亡率是因為Pancreatic cancer的轉移作用會造成其他器官病變導致有效診斷和治療的困難。在癌症轉移過程中特別需要基質金屬蛋白酶( Matrix metalloproteinase, MMP)的參與和協助，許多文獻顯示癌症腫瘤中MMP表達的量比起正常細胞或是良性腫瘤來的多很多。抑制MMP在治療癌症轉移時被視為一個重要的目標。
強力黴素（Doxycycline, DOX）可以降低口腔癌細胞株中MMP-9的表達量，口腔癌細胞加入TGF-β1後，能誘導MMP-9的表達，但也可以被Dox抑制。本研究以gelatinase—MMP-2為主要的研究目標，胰腺癌細胞株PANC-1會常態性表達MMP-2，但TGF-β1亦能誘導MMP-2表現量。研究目標是探討Dox是否也能抑制胰腺癌細胞株MMP-2的表達。除了使用Dox外，也使用了拔除其抗生素活性的Dox 衍生物TMC-1，觀察不具抗生素能力的四環黴素藥物是否也能抑制MMP-2的效果。
研究結果顯示胰腺癌細胞以Dox、TMC-1處理後可以有效抑制其MMP-2的表達，在明膠蛋白酵素電泳中可以觀察到40 μg/ml 的TMC-1和Dox均能抑制PANC-1的MMP-2表達量。在侵襲試驗中觀察到兩種藥物可以均可以抑制細胞侵襲，40 μg/ml TMC-1和Dox均具有anti-invasion的能力。這些實驗都顯示出Doxycycline和TMC-1可以藉由TGFβ-1 pathway 抑制 MMP-2的表達。

Our previous study discovered that inhibition of MMP-9 expression by Doxycycline (DOX) is through interfering of TGFβ-1 pathways. In order to confirm whether DOX can inhibit another gelatinase, MMP-2, we selected pancreatic cancer cell (PANC-1) as experimental target. We not only used DOX to inhibit MMP-2 expression but also used Tetracycline analog ,TMC-1, to inhibit MMP-2 expression. We found that both Dox and TMC-1 at 40 μg/ml could inhibit the expression of MMP-2 in PANC-1. We also found both Dox and TMC-1 at 40 μg/ml show significant anti-invassion activity of PANC-1. We conclude that both Dox and TMC-1 can inhibit the expression of MMP-2 and prevent the invasion of PANC-1 cells.

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