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首页> 外文期刊>Journal of experimental & clinical cancer research : >LINC00680 enhances hepatocellular carcinoma stemness behavior and chemoresistance by sponging miR-568 to upregulate AKT3
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LINC00680 enhances hepatocellular carcinoma stemness behavior and chemoresistance by sponging miR-568 to upregulate AKT3

机译：LINC00680通过海绵MIR-568增强肝细胞癌茎干行为和化学抑制，以上调AKT3

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Hepatocellular carcinoma (HCC) has an extremely poor prognosis due to the development of chemoresistance, coupled with inherently increased stemness properties. Long non-coding RNAs (LncRNAs) are key regulators for tumor cell stemness and chemosensitivity. Currently the relevance between LINC00680 and tumor progression was still largely unknown, with only one study showing its significance in glioblastoma. The study herein was aimed at identifying the role of LINC00680 in the regulation HCC stemness and chemosensitivity. QRT-PCR was used to detect the expression of LINC00680, miR-568 and AKT3 in tissue specimen and cell lines. Gain- or loss-of function assays were applied to access the function of LINC00680 in HCC cells, including cell proliferation and stemness properties. HCC stemness and chemosensitivity were determined by sphere formation, cell viability and colony formation. Luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays were performed to examine the interaction between LINC00680 and miR-568 as well as that between miR-568 and AKT3. A nude mouse xenograft model was established for the in vivo study. We found that LINC00680 was remarkably upregulated in HCC tissues. Patients with high level of LINC00680 had poorer prognosis. LINC00680 overexpression significantly enhanced HCC cell stemness and decreased in vitro and in vivo chemosensitivity to 5-fluorouracil (5-Fu), whereas LINC00680 knockdown led to opposite results. Mechanism study revealed that LINC00680 regulated HCC stemness and chemosensitivity through sponging miR-568, thereby expediting the expression of AKT3, which further activated its downstream signaling molecules, including mTOR, elF4EBP1, and p70S6K. LINC00680 promotes HCC stemness properties and decreases chemosensitivity through sponging miR-568 to activate AKT3, suggesting that LINC00680 might be a potentially important HCC diagnosis marker and therapeutic target.
机译：肝细胞癌（HCC）预后具有极低的预后，由于化学性的发展，与固有的茎秆特性相结合。长期非编码RNA（LNCRNA）是肿瘤细胞茎和化学敏感性的关键调节因子。目前，LINC00680与肿瘤进展之间的相关性仍然很大程度上是未知的，只有一项研究表明其在胶质母细胞瘤中的意义。本文的研究旨在鉴定LINC00680在监管HCC茎干和化学敏感度中的作用。 QRT-PCR用于检测组织样本和细胞系中LINC00680，MIR-568和AKT3的表达。应用功能测定的增益或丧失函数测定以进入HINC00680在HCC细胞中的功能，包括细胞增殖和茎秆特性。通过球形形成，细胞活力和菌落形成确定HCC茎和化学敏感性。进行荧光素酶报告器，RNA免疫沉淀（RIP）和RNA下拉测定以检查LINC00680和MIR-568之间的相互作用以及MIR-568和AKT3之间的相互作用。为体内研究建立了裸鼠异种移植模型。我们发现LINC00680在HCC组织中显着上调。 LINC00680水平高的患者预后较差。 LINC00680过表达显着增强了HCC细胞茎，体外和体内化学敏感性降低至5氟尿嘧啶（5-FU），而LINC00680敲低导致结果相反。机制研究表明，LINC00680通过海绵miR-568调节HCC茎干和化学敏感性，从而加速AKT3的表达，其进一步激活其下游信号分子，包括MTOR，ELF4EBP1和P70S6K。 LINC00680促进HCC茎秆特性，通过海绵MIR-568降低化学敏感性，以激活AKT3，表明LINC00680可能是潜在的重要HCC诊断标志物和治疗目标。

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