XB130 is a novel adapter protein that behaves as a tumor promoter or suppressor mediating cell proliferation and metastasis in the development of different human tumors. Altered expression of XB130 has been verified in human non‐small cell‐lung cancer (NSCLC). However, the exact effect of XB130 on NSCLC is not well‐understood. In this study, we investigated the biological function and posttranscriptional regulation of XB130 in NSCLC. First, the effects of XB130 silence on NSCLC cell proliferation, migration, invasion, and epithelial‐mesenchymal transition (EMT) were examined. Then the targeting relationship between XB130 and miR‐203, miR‐219, or miR‐4782‐3p was demonstrated by dual‐luciferase reporter assay. Finally, the effects of miR‐203, miR‐219, and miR‐4782‐3p on NSCLC cell function were studied, respectively. We found that XB130 silence significantly inhibited cell growth, migration and invasion, and reversed EMT. Furthermore, XB130 was posttranscriptionally regulated by miR‐203, miR‐219, and miR‐4782‐3p. Overexpression of miR‐203, miR‐219, or miR‐4782‐3p inhibited cell growth, migration and invasion, and reversed EMT, just like the role of XB130 in NSCLC cells, whereas the suppressive effects of microRNA (miRNA) overexpression were weakened by miRNA inhibitors or ectopic expression of XB130 in NSCLC cells. These data demonstrate that XB130 is posttranscriptionally regulated by miR‐203, miR‐219, and miR‐4782‐3p and mediates the proliferation and metastasis of NSCLC cells.

中文翻译：

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由miR-203，miR-219和miR-4782-3p调节的XB130介导非小细胞肺癌细胞的增殖和转移。

XB130是一种新型的衔接蛋白，在不同人类肿瘤的发生过程中，它起着肿瘤启动子或抑制剂的作用，介导细胞增殖和转移。XB130表达的改变已在人非小细胞肺癌（NSCLC）中得到证实。但是，XB130对NSCLC的确切作用尚不为人所理解。在这项研究中，我们调查了XB130在非小细胞肺癌中的生物学功能和转录后调控。首先，研究了XB130沉默对NSCLC细胞增殖，迁移，侵袭和上皮间质转化（EMT）的影响。然后通过双荧光素酶报告基因分析证明了XB130与miR-203，miR-219或miR-4782-3p之间的靶向关系。最后，分别研究了miR-203，miR-219和miR-4782-3p对NSCLC细胞功能的影响。我们发现XB130沉默显着抑制细胞生长，迁移和侵袭，并逆转EMT。此外，XB130在转录后受miR-203，miR-219和miR-4782-3p调控。就像XB130在NSCLC细胞中的作用一样，miR-203，miR-219或miR-4782-3p的过表达抑制细胞生长，迁移和侵袭，并逆转EMT，而microRNA（miRNA）的过表达抑制作用却减弱了通过miRNA抑制剂或XB130在NSCLC细胞中的异位表达。这些数据表明XB130受miR-203，miR-219和miR-4782-3p转录后调控，并介导NSCLC细胞的增殖和转移。就像XB130在NSCLC细胞中的作用一样，miR-203，miR-219或miR-4782-3p的过表达抑制细胞生长，迁移和侵袭，并逆转EMT，而microRNA（miRNA）的过表达抑制作用却减弱了通过miRNA抑制剂或XB130在NSCLC细胞中的异位表达。这些数据表明XB130受miR-203，miR-219和miR-4782-3p转录后调控，并介导NSCLC细胞的增殖和转移。就像XB130在NSCLC细胞中的作用一样，miR-203，miR-219或miR-4782-3p的过表达抑制细胞生长，迁移和侵袭，并逆转EMT，而microRNA（miRNA）的过表达抑制作用却减弱了通过miRNA抑制剂或XB130在NSCLC细胞中的异位表达。这些数据表明XB130受miR-203，miR-219和miR-4782-3p转录后调控，并介导NSCLC细胞的增殖和转移。