The matrix metalloproteinase-7 regulates the extracellular shedding of syndecan-2 from colon cancer cells
The matrix metalloproteinase-7 regulates the extracellular shedding of syndecan-2 from colon cancer cells
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DOI：
10.1016/j.bbrc.2011.12.120
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发表时间：
2012-01-27
影响因子：
3.1
通讯作者：
Oh, Eok-Soo
中科院分区：
文献类型：
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作者：
Choi, Sojoong;Kim, Jin-Yung;Oh, Eok-Soo
细胞表面硫酸乙酰肝素蛋白聚糖syndecan-2作为对接受体调节基质金属蛋白酶-7（MMP-7）的活化。在这里，我们证明了MMP-7对结肠癌细胞中多配体蛋白聚糖-2脱落的作用。Western印迹分析显示，在各种结肠癌细胞的培养基中发现了脱落的syndecan-2。MMP-7的过表达增强了多配体蛋白聚糖-2的脱落，而当使用小的抑制性RNA敲低MMP-7水平时，情况正好相反。一致的是，用MMP-7处理的HT 29细胞，而不是MMP-2或MMP-9，显示以时间和浓度依赖性方式增加脱落的syndecan-2。此外，MALDI-TOF MS分析和N-末端氨基酸测序显示，MMP-7在体外切割重组syndecan-2和内源性糖基化syndecan-2胞外域在N-末端的Lee残基。总之，数据表明MMP-7直接介导syndecan-2从结肠癌细胞脱落。(C)2011 Elsevier Inc. All rights reserved.
The cell surface heparan sulfate proteoglycan syndecan-2 regulates the activation of matrix metalloproteinase-7 (MMP-7) as a docking receptor. Here, we demonstrate the role of MMP-7 on syndecan-2 shedding in colon cancer cells. Western blot analysis showed that shed syndecan-2 was found in the culture media from various colon cancer cells. Overexpression of MMP-7 enhanced syndecan-2 shedding, whereas the opposite was true when MMP-7 levels were knocked-down using small inhibitory RNAs. Consistently, HT29 cells treated with MMP-7, but neither MMP-2 nor MMP-9, showed increased shed syndecan-2 in a time- and concentration-dependent manner. Furthermore, MALDI-TOF MS analysis and N-terminal amino acid sequencing revealed that MMP-7 cleaved both recombinant syndecan-2 and an endogenously glycosylated syndecan-2 ectodomain in the N-terminus at Lee residue in vitro. Taken together, the data suggest that MMP-7 directly mediates shedding of syndecan-2 from colon cancer cells. (C) 2011 Elsevier Inc. All rights reserved.