*3.1.1 Lung cancer*

In the last year, Ni et al. extracted exosomes from the plasma of non-small cell lung cancer (NSCLC) patients with or without bone metastasis. They found exosomal lncRNA-SOX2OT enhanced bone metastasis of NSCLC by targeting the miRNA-194-5p/RAC1 signaling axis in osteoclasts [93]. In organ-specific metastatic lung cancer cells, Ai et al. observed miR-660-5p involved tumor progression and bone-specific metastasis by nm23-H1/miR-660-5p/SMARCA5/RANKL axis [94]. Yang et al. identified an exosomal microRNA cluster that has an association with bone metastasis. Specifically, in this cluster miR-574-5p was down-regulated, miR-328-3p and miR-423-3p were up-regulated in patients with bone metastasis, which suppressed or activated the Wnt/β-catenin pathway [95]. Han et al. observed that upregulated miR-106a promoted bone metastasis by targeting tumor protein 53-induced nuclear protein 1 (TP53INP1), including cell migration, death, and EMT [96]. Xu et al. found miR-139-5p was downregulated in serum to facilitate lytic bone metastasis by targeting Notch1 [97]. In addition, miR-17-5p promotes osteoclastogenesis through the PI3K/Akt pathway via targeting PTEN [98]. Liu et al. revealed that miR-365 was reduced in patients with bone metastasis of NSCLC, and miR-365 could suppress lung metastasis via NKX2-1/EGFR/PI3K axis [99]. Zou et al.

demonstrated that increased miR-192-5p in patient serum inhibited lung cancer metastasis, possibly by reducing TRIM44 [100]. Loss of miR-886-3p expression was mediated by DNA hypermethylation of its promoter in both cultured small cell lung cancer (SCLC) cells and tumor samples. What's more, upregulated miR-886-3p greatly inhibited bone metastasis [101]. The downregulation of Wnt inhibitory factor 1 (WIF-1) expression was linked to hypermethylation of its promoter, which increased lung metastasis [102].

### *3.1.2 Liver cancer*

In liver cancer bone metastasis, Zhang et al. revealed the molecular function of lncRNA 34a regulated bone metastasis. Mechanistically, lncRNA 34a epigenetically suppressed miR-34a level via the recruitment of DNMT3a by Prohibitin 2 (PHB2) to methylate miR-34a promoter and histone deacetylase (HDAC) 1 to promote histones deacetylation. On the other hand, miR-34a regulated Smad4 through the transforming growth factor-β (TGF-β) pathway, impacting the downstream genes (i.e., connective tissue growth factor (CTGF) and IL-11) associated with bone metastasis [120]. Huang et al. identified lnRNA H19/p38 mitogen-activated protein kinase (MPAK)/ osteoprotegerin (OPG) and lncRNA H19/miR200b-3p/ZEB1 axes contributed to hepatocellular carcinoma bone metastasis [121].
