Our group previously found that LINC00665 was upregulated in hepatocellular carcinoma (HCC) tissues through database analysis; however, the potential molecular mechanism of LINC00665 in HCC progression still needs further study. qRTPCR was performed to determine the differential expression of LINC00665 and let-7i in HCC cells. Dual-luciferase reporter assays were performed to analyze the interaction of LINC00665 and let-7i. CCK-8 assays, scratch assays, Transwell invasion assays, qRTPCR and western blotting were performed to determine the regulatory mechanism of LINC00665/let-7i/HMGA1 in HCC cells. Animal tumorigenesis experiments were used to detect changes in tumor growth in nude mice after silencing LINC00665. LINC00665 was upregulated in HCC cells compared with normal hepatocytes. A potential binding site between LINC00665 and let-7i was confirmed by dual-luciferase reporter assay. In HCC cells, inhibition of LINC00665 significantly reduced cell proliferation, migration and invasion ability via the let-7i/HMGA1 signaling axis. LINC00665 promotes the proliferation and invasion of HCC cells via the let-7i/HMGA1 signaling axis.

中文翻译：

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LINC00665靶点let-7i/HMGA1促进肝癌细胞增殖和侵袭

我们课题组此前通过数据库分析发现LINC00665在肝细胞癌（HCC）组织中表达上调；然而，LINC00665在HCC进展中的潜在分子机制仍需进一步研究。进行qRTPCR以确定HCC细胞中LINC00665和let-7i的差异表达。进行双荧光素酶报告基因测定来分析 LINC00665 和 let-7i 的相互作用。通过CCK-8实验、划痕实验、Transwell侵袭实验、qRTPCR和蛋白质印迹实验来确定LINC00665/let-7i/HMGA1在HCC细胞中的调控机制。采用动物肿瘤发生实验检测沉默LINC00665后裸鼠肿瘤生长的变化。与正常肝细胞相比，LINC00665 在 HCC 细胞中表达上调。通过双荧光素酶报告基因测定证实了 LINC00665 和 let-7i 之间的潜在结合位点。在 HCC 细胞中，抑制 LINC00665 通过 let-7i/HMGA1 信号轴显着降低细胞增殖、迁移和侵袭能力。LINC00665 通过 let-7i/HMGA1 信号轴促进 HCC 细胞的增殖和侵袭。