020-38473605
据BBC报道，英国东英吉利亚大学（University of East Anglia）的科研人员和美国佛蒙特大学（University of Vermont）的科学家进行的研究显示，癌细胞所释放的基质金属蛋白酶-8（matrix metalloproteinase-8 enzyme，简称MMP-8）其实是在扮演着“好人”的角色，因为它会通知免疫系统癌细胞的位置。而拥有较多这种酶的乳腺癌患者，病情相比其他乳腺癌患者要缓和的多。
MMP-8酶一直被视为是“坏人”。先前的研究指出，乳腺癌细胞所释放的MMP-8酶会促进癌细胞的生长。英国癌症研究所的科学家表示，这项研究结果显示，科研人员或许能利用MMP-8酶来对抗乳腺癌。
率领研究团队的东英吉利亚大学生物科学学院Dylan Edwards教授在《生物化学杂志》（Journal of Biological Chemistry）中发表研究结果时指出，当乳腺癌细胞释放MMP-8酶时，它其实会产生两种炎症因子，即IL-6及IL-8，而早前的研究指出，这两种炎症因子会促进癌细胞生长。
Edwards说：“原本这两种炎症因子被视为是‘分子剪刀’（molecular scissors），会破坏细胞的骨架，为癌细胞进攻和扩散至人体其他器官清除障碍。可是我们发现，那些过度生产MMP-8酶的乳腺癌细胞并不能长久生存，因为MMP-8酶会导致癌细胞无法继续生长。我们认为，这类酶具有保护作用，因为它能够通知免疫系统去攻击肿瘤。”
他还指出，上世纪90年代，科研人员用专门能够阻止MMP-8酶的药物来治疗癌症，但以失败告终。如今，这项研究结果可解释为何当时那些药物并不管用。
科研人员目前还不清楚MMP-8酶是如何导致炎症因子IL-6及IL-8被激活的，有关答案对指导今后的研究将起到重要作用。
Matrix metalloproteinase-8 (collagenase-2) induces the expression of interleukins-6 and -8 in breast cancer cells
文献检索：Dylan R. Edwards et al.
Matrix metalloproteinase-8 (MMP-8) is a tumor suppressive protease that cleaves numerous substrates including matrix proteins and chemokines. In particular MMP-8 proteolytically activates interleukin-8 (IL-8) and thereby regulates neutrophil chemotaxis in vivo. We have explored the effects of expression of either a wild-type (wt) or catalytically inactive (E198A) mutant version of MMP-8 in human breast cancer cell lines. Analysis of serum-free conditioned media from three breast cancer cell lines (MCF-7, SK-BR-3 and MDA-MB-231) expressing wt MMP-8 revealed elevated levels of interleukin-6 (IL-6) and IL-8. This increase was mirrored at the mRNA level, and was dependent on MMP-8 catalytic activity. However, sustained expression of wt MMP-8 by breast cancer cells was non-permissive for long-term growth, as shown by reduced colony formation compared to cells expressing either control vector or E198A mutant MMP-8. In long term culture of transfected MDA-MB-231 cells expression of wt but not E198A mutant MMP8 was lost, with IL-6 and IL-8 levels returning to baseline. Rare clonal isolates of MDA-MB-231 cells expressing wt MMP-8 were generated and these showed constitutively high levels of IL-6 and IL-8, though production of the interleukins was no longer dependent upon MMP-8 activity. These studies support a causal connection between MMP-8 activity and the IL-6/IL-8 network, with an acute response to MMP-8 involving induction of the pro-inflammatory mediators, which may in part serve to compensate for the deleterious effects of MMP-8 on breast cancer cell growth. This axis may be relevant to the recognised ability of MMP-8 to orchestrate the innate immune system in inflammation in vivo.