MicroRNA (miR)-1298 is widely down-regulated in a variety of malignant tumors, which facilitates cell proliferation, invasiveness, and migration. However, the specific biological function of miR-1298 in bladder cancer (BC) is still unknown. Connexin 43 (Cx43) is often up-regulated in tumors. Identifying miRNAs that target Cx43 in the setting of BC will help to develop Cx43-based therapies for BC. In this study, the results demonstrated that the expression levels of miR-1298 and Cx43 were significantly down-regulated and up-regulated, respectively, in BC tissues. Overexpression of miR-1298 inhibited cell proliferation, migration, and invasiveness in two BC cell lines as determined using MTT assays, cell cycle assays, colony formation assays, Transwell assays, gelatin zymography, and Western blot. In addition, we found that miR-1298 decreased Cx43 expression by directly targeting the 3'-UTR. Further, we observed that the promotion of BC cell proliferation, migration, and invasiveness from Cx43 on could be partially attenuated by overexpressing miR-1298. Moreover, the protein expression of p-ERK was ameliorated after transfection with overexpressed-miR-1298. Knockdown of Cx43 reversed the promotion of cell migration and invasiveness due to decreased expression of miR-1298. All of the data from our study indicate that miR-1298 could be a diagnostic marker of BC and a potential therapeutic agent via inhibiting Cx43.

中文翻译：

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MicroRNA-1298-5p通过下调连接蛋白43抑制细胞增殖和对膀胱癌细胞的侵袭。

MicroRNA（miR）-1298在多种恶性肿瘤中被广泛下调，从而促进细胞增殖，侵袭性和迁移。但是，miR-1298在膀胱癌（BC）中的特定生物学功能仍然未知。连接蛋白43（Cx43）通常在肿瘤中上调。鉴定在BC环境中靶向Cx43的miRNA将有助于开发针对BC的基于Cx43的疗法。在这项研究中，结果表明，在BC组织中，miR-1298和Cx43的表达水平分别显着下调和上调。使用MTT分析，细胞周期分析，集落形成分析，Transwell分析，明胶酶谱分析和Western印迹测定，miR-1298的过表达抑制了两个BC细胞系中的细胞增殖，迁移和侵袭性。此外，我们发现miR-1298通过直接靶向3'-UTR降低了Cx43表达。此外，我们观察到过表达miR-1298可以部分减弱BC细胞从Cx43开始的增殖，迁移和侵袭性。此外，用过量表达的miR-1298转染后，p-ERK的蛋白表达得到改善。由于miR-1298的表达降低，Cx43的敲低逆转了细胞迁移和侵袭性的促进作用。我们研究的所有数据表明，miR-1298可能是BC的诊断标志物，并且可能是通过抑制Cx43的潜在治疗剂。用过量表达的miR-1298转染后，p-ERK的蛋白表达得到改善。由于miR-1298的表达降低，Cx43的敲低逆转了细胞迁移和侵袭性的促进作用。我们研究的所有数据表明，miR-1298可能是BC的诊断标志物，并且可能是通过抑制Cx43的潜在治疗剂。用过量表达的miR-1298转染后，p-ERK的蛋白表达得到改善。由于miR-1298的表达降低，Cx43的敲低逆转了细胞迁移和侵袭性的促进作用。我们研究的所有数据表明，miR-1298可能是BC的诊断标志物，并且可能是通过抑制Cx43的潜在治疗剂。