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一种组织蛋白酶 K 抑制剂在预防和治疗乳腺癌骨转移的临床前模型中的疗效。

Efficacy of a cathepsin K inhibitor in a preclinical model for prevention and treatment of breast cancer bone metastasis.

机构信息

Merck & Co. Inc., Whitehouse Station, New Jersey.

Inception Sciences Canada Inc., Vancouver, BC, Canada.

出版信息

Mol Cancer Ther. 2014 Dec;13(12):2898-909. doi: 10.1158/1535-7163.MCT-14-0253. Epub 2014 Sep 23.

Abstract

Cathepsin K (CatK) is essential for osteoclast-mediated bone resorption. CatK expression is also detected in breast cancer cells that metastasize to bone. Here, the CatK inhibitor L-235 dosed in prevention (10, 30, and 100 mg/kg, p.o., b.i.d.) or treatment regimen (30 mg/kg) was compared with the bisphosphonate zoledronic acid (ZOL, 7.5 μg/kg/wk, s.c.) in the intratibial injection model of MDA-MB-231 breast carcinoma in nude rats. Progression of osteolysis, skeletal tumor burden, and local metastasis was evaluated by radiography through 42 days and ex vivo μCT and histology. IHC and RT-PCR confirmed the increases in CatK protein and mRNA levels in human breast cancer primary and metastatic tumors. In the experimental model of breast cancer bone metastasis, L-235 dosed in preventive mode resulted in a dose-related reduction of osteolysis of 72%, 75%, and 87% respectively, compared with ZOL by 86% versus intact. Similarly, L-235 significantly reduced intratibial tumor volume by 29%, 40%, and 63%, respectively, compared with 56% by ZOL versus vehicle. Efficacy of L-235 and ZOL on reduction of osteolytic lesions and tumor burden was comparable in treatment versus preventive regimens. All L-235 doses inhibited cortical disruption and extraskeletal tumor growth to a level comparable with ZOL. Assessment of local metastasis demonstrated that treatment with the CatK inhibitor was more effective than ZOL in reducing breast cancer invasion. These data support the role of CatK in breast cancer skeletal growth and metastasis and CatK inhibitors may represent a novel oral therapy for treatment of metastatic breast cancer.

摘要

组织蛋白酶 K(CatK)对于破骨细胞介导的骨吸收至关重要。CatK 的表达也在转移到骨骼的乳腺癌细胞中被检测到。在这里,CatK 抑制剂 L-235 以预防(10、30 和 100mg/kg,口服,每天两次)或治疗方案(30mg/kg)给药,与双膦酸盐唑来膦酸(ZOL,7.5μg/kg/周,皮下)进行了比较,在裸鼠 MDA-MB-231 乳腺癌的胫骨内注射模型中。通过 42 天的放射摄影术、体外 μCT 和组织学评估溶骨性进展、骨骼肿瘤负担和局部转移。IHC 和 RT-PCR 证实了人乳腺癌原发和转移性肿瘤中 CatK 蛋白和 mRNA 水平的增加。在乳腺癌骨转移的实验模型中,与 ZOL 相比,L-235 以预防模式给药分别导致骨溶解减少 72%、75%和 87%,而 ZOL 减少 86%。同样,与载体相比,L-235 分别显著减少胫骨内肿瘤体积 29%、40%和 63%。与预防方案相比,L-235 和 ZOL 在减少溶骨性病变和肿瘤负担方面的疗效相当。所有 L-235 剂量均抑制皮质破坏和骨骼外肿瘤生长,与 ZOL 相当。局部转移评估表明,CatK 抑制剂的治疗比 ZOL 更有效地减少乳腺癌侵袭。这些数据支持 CatK 在乳腺癌骨骼生长和转移中的作用,CatK 抑制剂可能代表一种用于治疗转移性乳腺癌的新型口服治疗方法。

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