Cathepsin K cleavage of SDF-1α inhibits its chemotactic activity towards glioblastoma stem-like cells

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• 作者：Vashendriya V.V. Hira^a ; ^b ; ¹ ; ^{v.v.hira@amc.uva.nl} ; Ur&scaron ; ka Verbov&scaron ; ek^c ; ¹ ; Barbara Breznik^c ; ^d ; Matic Srdič^e ; Marko Novinec^e ; Hala Kakar^a ; Jill Wormer^a ; Britt Van der Swaan^a ; Brigita Lenarčič^e ; Luiz Juliano^f ; Shwetal Mehta^b ; Cornelis J.F. Van Noorden^a ; Tamara T. Lah^c ; ^d ; ^e
• 关键词：CatK ; cathepsin K ; CXCR4/7 ; C-X-C receptor type 4/7 ; GBM ; glioblastoma ; GSLC ; glioma stem-like cell ; HIF-1α ; hypoxia-inducible factor-1α ; HSC ; hematopoietic stem cell ; IHC ; immunohistochemistry ; SDF-1α ; stromal-derived factor-1α ; VEGF ; vascular endothelial growth factor
• 刊名：Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
• 出版年：2017
• 出版时间：March 2017
• 年：2017
• 卷：1864
• 期：3
• 页码：594-603
• 全文大小：1535 K
• 卷排序：1864

文摘

Cysteine protease cathepsin K (CatK) cleaves and inactivates the chemokine SDF-1α. CatK cleavage products of SDF-1α impair invasion of GSLCs in vitro. CXCR4 inhibitor plerixafor inhibits invasion of GSLCs in vitro. CatK and SDF-1α colocalize in glioma stem-like cell niches in glioblastoma tissue. CatK activity can prevent homing of GSLCs to their therapy-protective niches.