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首页> 外文期刊>Journal of International Medical Research >SPOCD1 regulated by miR-133a-3p promotes hepatocellular carcinoma invasion and metastasis
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SPOCD1 regulated by miR-133a-3p promotes hepatocellular carcinoma invasion and metastasis

机译：miR-133a-3p调节的spocd1促进肝细胞癌侵袭和转移

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Objective To investigate the tumorigenic role of spen paralogue and orthologue C-terminal domain-containing 1 (SPOCD1) in hepatocellular carcinoma (HCC) and identify the upstream regulatory mechanism. Methods We analyzed SPOCD1 and miR-133-3p expression in normal and HCC tissues from the Cancer Genome Atlas and UALCAN databases, and in normal hepatocytes and HCC cell lines by real-time quantitative polymerase chain reaction and western blot. We identified the miR-133a-3p-binding site on the SPOCD1 3?-untranslated region using TargetScan. Hierarchical regulation was confirmed by luciferase assay and miR-133a-3p overexpression/silencing. Cell proliferation, migration, invasion, and colony formation were assessed by MTT, scratch, transwell, and clonogenic assays, respectively. Results SPOCD1 was highly expressed in HCC tissues and cell lines, while miR-133a-3p expression was significantly downregulated. Kaplan–Meier analysis indicated that high SPOCD1 expression was significantly associated with poor survival. TargetScan and luciferase reporter assay revealed that SPOCD1 was the downstream target of miR-133a-3p. Overexpression of miR-133a-3p significantly inhibited the expression of SPOCD1, while miR-133a-3p knockdown significantly increased SPOCD1 expression. Conclusion SPOCD1, regulated by miR-133a-3p, promotes HCC cell proliferation, migration, invasion, and colony formation. This study provides the first evidence for the role of the miR-133a-3p/SPOCD1 axis in HCC tumorigenesis.
机译：目的探讨Spen副病毒和直域C-末端结构域1（SPOCD1）在肝细胞癌（HCC）中的致瘤作用，并确定上游调节机制。方法通过实时定量聚合酶链反应和Western印迹分析来自癌症基因组Atlas和ualcan数据库的正常和HCC组织中的SpoCD1和MiR-133-3P表达，以及正常的肝细胞和HCC细胞系。我们使用TargetScan鉴定了Spocd1 3α-undranslated区域上的miR-133a-3p结合位点。通过荧光素酶测定和miR-133a-3p过表达/沉默证实了分层调节。通过MTT，划痕，Transwell和克隆灭绝测定细胞增殖，迁移，侵袭和菌落形成。结果SPOCD1在HCC组织和细胞系中高度表达，而MIR-133A-3P表达明显下调。 Kaplan-Meier分析表明，高Spocd1表达显着与差的存活率有关。 TargetScan和Luciferase报告器测定显示，Spocd1是miR-133a-3p的下游靶标。 miR-133a-3p的过度表达显着抑制了Spocd1的表达，而MiR-133A-3P敲低显着增加了SpoCD1表达。结论SPOCD1，MIR-133A-3P调节，促进了HCC细胞增殖，迁移，侵袭和菌落形成。本研究提供了MIR-133A-3P / SPOCD1轴在HCC肿瘤发生中的作用的第一种证据。

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