Fig 1: Schematic overview of the role of miR106a in lung cancer with bone metastasis.In response to diverse stresses, p53 was phosphorylated at Ser-46 and activate TP53INP1 signalling, which was involved in the cellular physiological process through a feedback loop: the phosphorylation of p53 at Ser-46 regulates TP53INP1 expression, and TP53INP3 regulates p53 activity via increasing the phosphorylation level of p53 at Ser-46. Subsequently, TP53INP1 could affect lung adenocarcinoma bone metastasis through three different ways: (1) TP53INP1 affects the expression of downstream target genes of p53, including p21, Pig3 and Bax; (2) TP53INP1 could displace p62 and form autophagosomes with LC3, which induces autophagy-dependent cell death; (3) TP53INP1 mediated EMT via regulating Smad2/3 signalling. As a TP53INP1 regulator, miR-106a enhances tumour survival and metastasis in different ways: (1) it inhibits TP53INP1 induced autophagy-dependent death; (2) it antagonizes the inhibition role of TP53INP1 on EMT.