Background

Hepatocellular carcinoma (HCC) is the sixth most commonly diagnosed malignant tumor and the fourth leading cause of cancer-related deaths worldwide. As a novel non-coding RNA, LINC00657 was firstly identified as an oncogenic role in breast cancer. However, few research focus on the effect of LINC00657 on the progression of HCC.

Objectives

The purpose of this study was to investigate the effect of LINC00657 on HCC tissues and cells, and further explore the potential mechanism.

Methods

We first measured the expression of LINC00657 in HCC tissues and cell lines using qRT-PCR. Next we established LINC00657 knockdown in HCC cells. CCK-8 assay, cell invasion assay, flow cytometry analysis, qRT-PCR and western blotting were applied to assess the role of LINC00657 knockdown in the biological behavior of HCC cells. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism.

Results

LINC00657 was remarkably overexpressed in HCC tissues and cell lines, associated with poor prognosis. LINC00657 knockdown repressed cell proliferation and invasion, promoted cell apoptosis of HCC cell lines. The bioinformatics analysis showed LINC00657 sponged miR-424 as a ceRNA. Besides, PD-L1 mimic rescued the suppression of si-LINC00657 in the biological behavior of HCC cells.

Conclusion

In a word, we observed LINC00657 regulated PD-L1 expression by sponging miR-424, thus affecting the developments of hepatocellular carcinoma. These findings LINC00657 may provide new evidence for therapeutic application in hepatocellular carcinoma.

中文翻译：

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LINC00657敲低通过海绵miR-424调节PD-L1表达抑制肝细胞癌进展

背景

肝细胞癌（HCC）是全球第六大最常见的恶性肿瘤，也是全球癌症相关死亡的第四大原因。作为一种新型的非编码 RNA，LINC00657 首次被鉴定为在乳腺癌中具有致癌作用。然而，很少有研究关注 LINC00657 对 HCC 进展的影响。

目标

本研究旨在探讨LINC00657对HCC组织和细胞的影响，并进一步探讨其潜在机制。

方法

我们首先使用 qRT-PCR 测量了 LINC00657 在 HCC 组织和细胞系中的表达。接下来，我们在 HCC 细胞中建立了 LINC00657 敲低。应用CCK-8测定、细胞侵袭测定、流式细胞术分析、qRT-PCR和蛋白质印迹来评估LINC00657敲低在HCC细胞生物学行为中的作用。生物信息学分析和救援实验致力于潜在机制。

结果

LINC00657 在 HCC 组织和细胞系中显着过表达，与不良预后相关。LINC00657敲低抑制细胞增殖和侵袭，促进HCC细胞系的细胞凋亡。生物信息学分析显示 LINC00657 将 miR-424 作为 ceRNA。此外，PD-L1 模拟物挽救了 si-LINC00657 在 HCC 细胞生物学行为中的抑制作用。

结论

总之，我们观察到LINC00657通过海绵miR-424调节PD-L1表达，从而影响肝细胞癌的发展。这些发现 LINC00657 可能为肝细胞癌的治疗应用提供新的证据。