Department of Orthopedics, The Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong, 515041, China.
Research Centre for Regenerative Medicine, The First Affiliated Hospital of Guangxi Medical University, Guangxi Medical University, Guangxi, 530021, China; Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Guangxi, 530021, China.
Cancer Lett. 2019 Feb 28;443:135-144. doi: 10.1016/j.canlet.2018.11.038. Epub 2018 Dec 9.
Bone metastasis causes bone pain and pathological bone fracture in breast cancer patients with a serious complication. Previous studies have demonstrated that a novel phosphatidyl inositol 3-kinase (PI3K)-mTOR inhibitor PKI-402 suppressed the growth of breast cancer cells. However, the role of PKI-402 involved in osteolysis induced by breast cancer remains unclear. In this study, we showed that treatment of PKI-402 led to significant decreases in RANKL-induced osteoclastogenesis and osteoclast-specific gene expression in mouse bone marrow-derived macrophages and reduced proliferation, migration and invasion of MDA-MB-231 breast cancer cells by blocking the PI3K-AKT-mTOR signaling pathway. Importantly, as evidenced by the observation that the administration of PKI-402 inhibited MDA-MB-231-induced osteolysis in vivo, PKI-402 exerted an inhibitory effect on osteoclast formation and bone resorption, critical for cancer cells-induced bone destruction. These results strongly suggest that PKI-402 might have a therapeutic potential to inhibit breast cancer induced osteolysis.
骨转移会导致乳腺癌患者出现骨痛和病理性骨折等严重并发症。先前的研究表明,一种新型的磷脂酰肌醇 3-激酶(PI3K)-哺乳动物雷帕霉素靶蛋白(mTOR)抑制剂 PKI-402 能够抑制乳腺癌细胞的生长。然而,PKI-402 抑制乳腺癌诱导的溶骨作用的机制尚不清楚。在本研究中,我们发现 PKI-402 处理能够显著抑制 RANKL 诱导的小鼠骨髓来源巨噬细胞中的破骨细胞生成和破骨细胞特异性基因表达,并通过阻断 PI3K-AKT-mTOR 信号通路抑制 MDA-MB-231 乳腺癌细胞的增殖、迁移和侵袭。重要的是,PKI-402 抑制 MDA-MB-231 诱导的体内溶骨作用的观察结果表明,PKI-402 对破骨细胞形成和骨吸收具有抑制作用,这对于癌细胞诱导的骨破坏至关重要。这些结果强烈表明,PKI-402 可能具有抑制乳腺癌诱导的溶骨作用的治疗潜力。