Hepatocellular carcinoma (HCC) remains one of the most common malignant tumors worldwide. This study aimed to investigate the biological role of microRNA-183-5p (miR-183-5p), a novel tumor-related miRNA, in HCC and illuminate the possible molecular mechanisms. The expression patterns of miR-183-5p in clinical samples were characterized using qPCR analysis. Kaplan-Meier survival curve was applied to evaluate the correlation between miR-183-5p expression and overall survival of HCC patients. Effects of miR-183-5p knockdown on HCC cell proliferation, apoptosis, migration and invasion capabilities were determined via CCK8 assays, flow cytometry, scratch wound healing assays and Transwell invasion assays, respectively. Mouse neoplasm transplantation models were established to assess the effects of miR-183-5p knockdown on tumor growth in vivo. Bioinformatics analysis, dual-luciferase reporter assays and rescue assays were performed for mechanistic researches. Results showed that miR-183-5p was highly expressed in tumorous tissues compared with adjacent normal tissues. Elevated miR-183-5p expression correlated with shorter overall survival of HCC patients. Moreover, miR-183-5p knockdown significantly suppressed proliferation, survival, migration and invasion of HCC cells compared with negative control treatment. Consistently, miR-183-5p knockdown restrained tumor growth in vivo. Furthermore, programmed cell death factor 4 (PDCD4) was identified as a direct target of miR-183-5p. Additionally, PDCD4 down-regulation was observed to abrogate the inhibitory effects of miR-183-5p knockdown on malignant phenotypes of HCC cells. Collectively, our data suggest that miR-183-5p may exert an oncogenic role in HCC through directly targeting PDCD4. The current study may offer some new insights for understanding the role of miR-183-5p in HCC.

中文翻译：

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MicroRNA-183-5p通过靶向人肝细胞癌中的PDCD4促进恶性进展。

肝细胞癌（HCC）仍然是全球最常见的恶性肿瘤之一。这项研究旨在研究新型的与肿瘤相关的miRNA microRNA-183-5p（miR-183-5p）在肝癌中的生物学作用，并阐明可能的分子机制。使用qPCR分析表征临床样品中miR-183-5p的表达模式。应用Kaplan-Meier生存曲线评估miR-183-5p表达与HCC患者总生存之间的相关性。分别通过CCK8测定，流式细胞术，刮擦伤口愈合测定和Transwell侵袭测定来确定miR-183-5p敲低对HCC细胞增殖，凋亡，迁移和侵袭能力的影响。建立小鼠肿瘤移植模型以评估miR-183-5p敲低对体内肿瘤生长的影响。进行了生物信息学分析，双荧光素酶报告基因分析和拯救分析，以进行机理研究。结果表明，与邻近的正常组织相比，miR-183-5p在肿瘤组织中高表达。miR-183-5p表达升高与肝癌患者总体生存期缩短有关。此外，与阴性对照治疗相比，miR-183-5p敲低显着抑制了HCC细胞的增殖，存活，迁移和侵袭。一致地，miR-183-5p敲低抑制了体内肿瘤的生长。此外，程序性细胞死亡因子4（PDCD4）被确定为miR-183-5p的直接靶标。此外，观察到PDCD4下调消除了miR-183-5p敲低对HCC细胞恶性表型的抑制作用。总的来说，我们的数据表明，miR-183-5p可能通过直接靶向PDCD4在HCC中发挥致癌作用。当前的研究可能为理解miR-183-5p在肝癌中的作用提供一些新的见解。