Department of Liver & Laparoscopic Surgery, Digestive & Vascular Surgery Center, The First Affiliated Hospital of Xinjiang Medical University, No. 137, Liyushan South Road, Xinshi District, Ürümqi, 830054, Xinjiang Uyghur Autonomous Region, China.
Department of Proctology, Xinjiang General Hospital of People's Liberation Army, Ürümqi, 830000, Xinjiang Uyghur Autonomous Region, China.
Genes Genomics. 2020 Nov;42(11):1361-1368. doi: 10.1007/s13258-020-01001-y. Epub 2020 Sep 29.
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.
The purpose of this study was to investigate the effect of LINC00657 on HCC tissues and cells, and further explore the potential mechanism.
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.
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.
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.
肝细胞癌（HCC）是全球第六种最常见的恶性肿瘤，也是第四大癌症相关死亡原因。作为一种新型非编码 RNA，LINC00657 最初被鉴定为乳腺癌的致癌基因。然而，很少有研究关注 LINC00657 对 HCC 进展的影响。
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。
我们首先使用 qRT-PCR 测量 HCC 组织和细胞系中 LINC00657 的表达。接下来，我们在 HCC 细胞中建立 LINC00657 敲低。CCK-8 测定、细胞侵袭测定、流式细胞术分析、qRT-PCR 和 Western blot 用于评估 LINC00657 敲低对 HCC 细胞生物学行为的作用。生物信息学分析和挽救实验致力于潜在机制的研究。
LINC00657 在 HCC 组织和细胞系中显著过表达，与预后不良相关。LINC00657 敲低抑制 HCC 细胞系的细胞增殖和侵袭，促进细胞凋亡。生物信息学分析表明 LINC00657 作为 ceRNA 吸附 miR-424。此外，PD-L1 模拟物挽救了 si-LINC00657 对 HCC 细胞生物学行为的抑制作用。
总之，我们观察到 LINC00657 通过吸附 miR-424 调节 PD-L1 的表达，从而影响肝细胞癌的发生发展。这些发现 LINC00657 可能为肝细胞癌的治疗应用提供新的证据。
