Department of Orthopedics, The Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong, China.
Institute of Translational Medicine, Shanghai University, Shanghai, China.
Biochem Pharmacol. 2021 Jun;188:114579. doi: 10.1016/j.bcp.2021.114579. Epub 2021 Apr 23.
Osteolytic diseases, including breast cancer-induced osteolysis and postmenopausal osteoporosis, are attributed to excessive bone resorption by osteoclasts. Spleen tyrosine kinase (SYK) is involved in osteoclastogenesis and bone resorption, whose role in breast cancer though remains controversial. Effects of PRT062607 (PRT), a highly specific inhibitor of SYK, on the osteoclast and breast cancer functionalities are yet to be clarified. This study demonstrated the in vitro inhibitory actions of PRT on the osteoclast-specific gene expression, bone resorption, and osteoclastogenesis caused by receptor activator of nuclear factor kappa B ligand (RANKL), as well as its in vitro suppressive effects on the growth, migration and invasion of breast carcinoma cell line MDA-MB-231, which were achieved through PLCγ2 and PI3K-AKT-mTOR pathways. Further, we proved that PRT could prevent post-ovariectomy (OVX) loss of bone and breast cancer-induced bone destruction in vivo, which agreed with the in vitro outcomes. In conclusion, our findings suggest the potential value of PRT in managing osteolytic diseases mediated by osteoclasts.
溶骨性疾病,包括乳腺癌诱导的溶骨性骨病和绝经后骨质疏松症,归因于破骨细胞的过度骨吸收。脾酪氨酸激酶(SYK)参与破骨细胞的生成和骨吸收,其在乳腺癌中的作用仍存在争议。PRT062607(PRT)是一种 SYK 的高度特异性抑制剂,其对破骨细胞和乳腺癌功能的影响尚不清楚。本研究表明 PRT 在体外对核因子κB 受体激活剂配体(RANKL)诱导的破骨细胞特异性基因表达、骨吸收和破骨细胞生成具有抑制作用,以及通过 PLCγ2 和 PI3K-AKT-mTOR 通路对乳腺癌细胞系 MDA-MB-231 的生长、迁移和侵袭的体外抑制作用。此外,我们证明 PRT 可以预防卵巢切除术后(OVX)骨丢失和体内乳腺癌诱导的骨破坏,这与体外结果一致。总之,我们的研究结果表明 PRT 在治疗由破骨细胞介导的溶骨性疾病方面具有潜在价值。