| Literature DB >> 30540926 |
Guixin Yuan1, Zhen Lian1, Qian Liu2, Xixi Lin2, Dantao Xie1, Fangming Song2, Xinjia Wang1, Siyuan Shao2, Bo Zhou3, Chen Li2, Muyan Li4, Guanfeng Yao5.
Abstract
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.Entities:
Keywords: Bone destruction; Bone metastasis; MDA-MB-231 cells; Osteoclast; PI3K-mTOR-AKT-Signaling pathway
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Year: 2018 PMID: 30540926 DOI: 10.1016/j.canlet.2018.11.038
Source DB: PubMed Journal: Cancer Lett ISSN: 0304-3835 Impact factor: 8.679