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首页> 外文期刊>Cellular Physiology and Biochemistry >Long Noncoding RNA AFAP1-AS1 Promoted Tumor Growth and Invasion in Cholangiocarcinoma
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Long Noncoding RNA AFAP1-AS1 Promoted Tumor Growth and Invasion in Cholangiocarcinoma

机译：长非编码RNA AFAP1-AS1促进胆管癌的肿瘤生长和侵袭。

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>Background: Long non-coding RNAs (lncRNAs) have been shown to play important roles in a wide range of pathophysiological processes, including cancer progression. Our previous study has shown that AFAP1-AS1 was upregulated and acted as an oncogene in hepatocellular carcinoma. However, the expression and biological functions of lncRNA AFAP1-AS1 in intrahepatic cholangiocarcinoma (CCA) remains largely unknown. Methods: The expression level of AFAP1-AS1 was measured in 56 pairs of human cholangiocarcinoma tumor tissues and corresponding adjacent normal bile duct tissues. The correlation between AFAP1-AS1 and the clinicopathological features were evaluated by chi-square test. The effects of AFAP1-AS1 on CCA cells were determined by CCK-8 assay, clone formation assay, flow cytometry and transwell assay. Finally, to determine the effect of AFAP1-AS1 on tumor growth in vivo, AFAP1-AS1 knockdowned CCLP-1 cells were subcutaneously into nude mice to evaluate tumor growth. Results: In this study, we found that lncRNA AFAP1-AS1 was increased in CCA tissues and patients with high AFAP1-AS1 expression had a shorter overall survival. SiRNA-mediated AFAP1-AS1 knockdown significantly decreased cell proliferation of the CCA cells, with downregulation of C-myc and Cycling D1 in vitro. Furthermore, AFAP1-AS1 silencing inhibited cell migration partly due to decrease the expression of MMP-2 and MMP-9. In addition, CCLP-1 cells with AFAP1-AS1 knockdown were injected into nude mice to investigate the effect of AFAP1-AS1 on the tumorigenesis in vivo. Conclusions: Taken together, our findings suggested that AFAP1-AS1 might promote the CCA progression and provided a novel potential therapeutic target for CCA.
机译：> 背景： 长非编码RNA（lncRNA）已被证明在包括癌症进展在内的各种病理生理过程中都起着重要作用。我们以前的研究表明，AFAP1-AS1在肝细胞癌中被上调并作为癌基因。然而，lncRNA AFAP1-AS1在肝内胆管癌（CCA）中的表达和生物学功能仍然未知。 方法： 在56对人胆管癌肿瘤组织和相应的邻近正常胆管组织中检测AFAP1-AS1的表达水平。通过卡方检验评估AFAP1-AS1与临床病理特征之间的相关性。通过CCK-8测定，克隆形成测定，流式细胞术和transwell测定来确定AFAP1-AS1对CCA细胞的作用。最后，为了确定AFAP1-AS1对体内肿瘤生长的影响，将敲低AFAP1-AS1的CCLP-1细胞皮下植入裸鼠以评估肿瘤的生长。 结果： 在这项研究中，我们发现CCA组织中的lncRNA AFAP1-AS1增加，而AFAP1-AS1高表达的患者的总生存期较短。 SiRNA介导的AFAP1-AS1敲低显着降低了CCA细胞的细胞增殖，并在体外下调了C-myc和Cycling D1。此外，AFAP1-AS1沉默部分抑制了细胞迁移，这是由于降低了MMP-2和MMP-9的表达。此外，将具有AFAP1-AS1基因敲低的CCLP-1细胞注入裸鼠，以研究AFAP1-AS1对体内肿瘤发生的影响。 结论： 总之，我们的发现表明AFAP1-AS1可能促进CCA的进展，并为CCA提供了新的潜在治疗靶标。

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