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DASH蛋白酶抑制剂影响破骨细胞中黏附分子的表达,并减少骨髓瘤生长和骨病。

Inhibitor of DASH proteases affects expression of adhesion molecules in osteoclasts and reduces myeloma growth and bone disease.

作者信息

Pennisi Angela, Li Xin, Ling Wen, Khan Sharmin, Gaddy Dana, Suva Larry J, Barlogie Bart, Shaughnessy John D, Aziz Nazneen, Yaccoby Shmuel

机构信息

Myeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

出版信息

Br J Haematol. 2009 Jun;145(6):775-87. doi: 10.1111/j.1365-2141.2009.07696.x. Epub 2009 Apr 8.

Abstract

Dipeptidyl peptidase (DPP) IV activity and/or structure homologues (DASH) are serine proteases implicated in tumourigenesis. We previously found that a DASH protease, fibroblast activation protein (FAP), was involved in osteoclast-induced myeloma growth. Here we further demonstrated expression of various adhesion molecules in osteoclasts cultured alone or cocultured with myeloma cells, and tested the effects of DASH inhibitor, PT-100, on myeloma cell growth, bone disease, osteoclast differentiation and activity, and expression of adhesion molecules in osteoclasts. PT-100 had no direct effects on viability of myeloma cells or mature osteoclasts, but significantly reduced survival of myeloma cells cocultured with osteoclasts. Real-time PCR array for 85 adhesion molecules revealed upregulation of 17 genes in osteoclasts after coculture with myeloma cells. Treatment of myeloma/osteoclast cocultures with PT-100 significantly downregulated 18 of 85 tested genes in osteoclasts, some of which are known to play roles in tumourigenesis and osteoclastogenesis. PT-100 also inhibited osteoclast differentiation and subsequent pit formation. Resorption activity of mature osteoclasts and differentiation of osteoblasts were not affected by PT-100. In primary myelomatous severe combined immunodeficient (SCID)-hu mice PT-100 reduced osteoclast activity, bone resorption and tumour burden. These data demonstrated that DASH proteases are involved in myeloma bone disease and tumour growth.

摘要

二肽基肽酶(DPP)IV活性和/或结构同源物(DASH)是与肿瘤发生有关的丝氨酸蛋白酶。我们之前发现一种DASH蛋白酶,即成纤维细胞活化蛋白(FAP),参与破骨细胞诱导的骨髓瘤生长。在此,我们进一步证明了单独培养或与骨髓瘤细胞共培养的破骨细胞中各种粘附分子的表达,并测试了DASH抑制剂PT - 100对骨髓瘤细胞生长、骨病、破骨细胞分化和活性以及破骨细胞中粘附分子表达的影响。PT - 100对骨髓瘤细胞或成熟破骨细胞的活力没有直接影响,但显著降低了与破骨细胞共培养的骨髓瘤细胞的存活率。针对85种粘附分子的实时PCR阵列显示,破骨细胞与骨髓瘤细胞共培养后,有17个基因上调。用PT - 100处理骨髓瘤/破骨细胞共培养物可显著下调破骨细胞中85个测试基因中的18个,其中一些已知在肿瘤发生和破骨细胞生成中起作用。PT - 100还抑制破骨细胞分化和随后的蚀斑形成。PT - 100不影响成熟破骨细胞的吸收活性和成骨细胞的分化。在原发性骨髓瘤严重联合免疫缺陷(SCID)-人源化小鼠中,PT - 100降低了破骨细胞活性、骨吸收和肿瘤负荷。这些数据表明,DASH蛋白酶参与了骨髓瘤骨病和肿瘤生长。

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