Institute for Advancing Translational Medicine in Bone &Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Institute of Integrated Bioinfomedicine and Translational Science, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.
Sci Rep. 2017 Jan 10;7:40487. doi: 10.1038/srep40487.
The role of osteoclastic miRNAs in regulating osteolytic bone metastasis (OBM) of breast cancer is still underexplored. Here, we examined the expression profiles of osteoclastogenic miRNAs in human bone specimens and identified that miR-214-3p was significantly upregulated in breast cancer patients with OBM. Consistently, we found increased miR-214-3p within osteoclasts, which was associated with the elevated bone resorption, during the development of OBM in human breast cancer xenografted nude mice (BCX). Furthermore, genetic ablation of osteoclastic miR-214-3p in nude mice prevent the development of OBM. Conditioned medium from MDA-MB-231 cells dramatically stimulated miR-214-3p expression to promote osteoclast differentiation. Mechanistically, a series of in vitro study showed that miR-214-3p directly targeted Traf3 to promote osteoclast activity and bone-resorbing activity. In addition, osteoclast-specific miR-214-3p knock-in mice showed remarkably increased bone resorption when compared to the littermate controls, which was attenuated after osteoclast-targeted treatment with Traf3 3'UTR-containing plasmid. In BCX nude mice, osteoclast-targeted antagomir-214-3p delivery could recover the TRAF3 protein expression and attenuate the development of OBM, respectively. Collectively, inhibition of osteoclastic miR-214-3p may be a potential therapeutic strategy for breast cancer patients with OBM. Meanwhile, the intraosseous TRAF3 could be a promising biomarker for evaluation of the treatment response of antagomir-214-3p.
破骨细胞 miRNA 在调节乳腺癌溶骨性骨转移(OBM)中的作用仍未得到充分探索。在这里,我们检测了人骨标本中破骨细胞生成性 miRNA 的表达谱,发现 miR-214-3p 在乳腺癌伴 OBM 患者中显著上调。一致地,我们发现,在人乳腺癌异种移植裸鼠(BCX)中 OBM 发展过程中,破骨细胞内 miR-214-3p 增加,与骨吸收增加相关。此外,裸鼠中破骨细胞 miR-214-3p 的遗传缺失可预防 OBM 的发生。MDA-MB-231 细胞的条件培养基可显著刺激 miR-214-3p 的表达,从而促进破骨细胞分化。从机制上讲,一系列体外研究表明,miR-214-3p 可直接靶向 Traf3 以促进破骨细胞活性和骨吸收活性。此外,与同窝对照相比,破骨细胞特异性 miR-214-3p 敲入小鼠的骨吸收明显增加,而经破骨细胞靶向 Traf3 3'UTR 载体制剂治疗后则减轻。在 BCX 裸鼠中,破骨细胞靶向 antagomir-214-3p 递送可分别恢复 TRAF3 蛋白表达并减轻 OBM 的发生。总之,抑制破骨细胞 miR-214-3p 可能是治疗乳腺癌伴 OBM 患者的一种潜在治疗策略。同时,骨内 TRAF3 可能是评估 antagomir-214-3p 治疗反应的有前途的生物标志物。