MicroRNAs (miRNAs) can function as tumor suppressor or oncogenic genes. The putative targets of miR-223 include tumor suppressor gene, RhoB. Here we sought to investigate the role of miR-223-RhoB signaling pathway in proliferation of colon cancer. We used Western blot, immunofluorescence staining, or RT-PCR to detect expression levels of miR-223 and RhoB in colon adenocarcinoma and adjacent non-cancerous tissue samples, or in human colon adenocarcinoma cell lines. MTT assay was used to determine proliferation and apoptosis in cell lines. We further used Western blot to determine levels of cell cycle regulators CDK1 and Cyclin B1 with anti-miR-223 or apoptosis with overexpression of RhoB. The expression level of miR-223 was significantly upregulated in clinical samples and cell lines of colon adenocarcinoma, in contrast to down-regulation of RhoB. In addition, we showed that inhibition of miR-223 led to upregulation of RhoB and in turn suppression of proliferation of colon adenocarcinoma. Moreover, inhibition of miR-223 or overexpression of RhoB induced cell arrest or apoptosis in colon adenocarcinoma. These results suggest that miR-223-RhoB signaling pathway plays an important role in modulation of proliferation, cell arrest, and apoptosis in colon cancer.

微小RNA（miRNA）可以充当抑癌基因或致癌基因。miR-223的假定靶标包括肿瘤抑制基因RhoB。在这里，我们试图研究miR-223-RhoB信号通路在结肠癌增殖中的作用。我们使用蛋白质印迹，免疫荧光染色或RT-PCR来检测miR-223和RhoB在结肠腺癌和邻近的非癌组织样品中或在人类结肠腺癌细胞系中的表达水平。使用MTT测定法确定细胞系中的增殖和凋亡。我们进一步使用蛋白质印迹来确定具有抗miR-223的细胞周期调节剂CDK1和细胞周期蛋白B1的水平或RhoB过表达的细胞凋亡。与RhoB的下调相反，在结肠腺癌的临床样品和细胞系中，miR-223的表达水平显着上调。此外，我们表明抑制miR-223导致RhoB的上调，进而抑制结肠腺癌的增殖。此外，在结肠腺癌中，miR-223的抑制或RhoB的过度表达诱导细胞停滞或凋亡。这些结果表明，miR-223-RhoB信号通路在结肠癌的增殖，细胞停滞和凋亡的调节中起重要作用。