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<p>Hepatocellular carcinoma (HCC) is a major cause of cancer death globally, with a poor prognosis. The long non-coding RNA <i>TUG1</i> has been implicated, but its specific role in HCC remains unclear. RT-qPCR was used to evaluate <i>TUG1</i> and <i>PD-L1</i> expression, while GEO and TCGA databases were utilized to compare <i>TUG1</i> levels between HCC patients and healthy controls. In vitro, including CCK8, colony formation, and transwell, assessed cell growth. CD8 + T cell cytotoxicity was evaluated through HCC cells co-culture experiments, and the interaction of miR-377-3p with <i>TUG1</i> and <i>PD-L1</i> was examined using dual-luciferase reporter assays. Results indicated that <i>TUG1</i> was upregulated in HCC, particularly in advanced-stage disease, and PD-L1 expression positively correlated with <i>TUG1</i> levels. Notably, lenvatinib (LEN) treatment downregulated both <i>TUG1</i> and PD-L1 in HCC cells, enhancing CD8 + T cell-mediated cytotoxicity. Overexpression of <i>TUG1</i> diminished the efficacy of LEN, while <i>TUG1</i> knockdown enhanced it. Mechanistically, <i>TUG1</i> was found to sponge miR-377-3p, thereby increasing <i>PD-L1</i> expression. In vivo, <i>TUG1</i> knockdown combined with LEN treatment significantly reduced tumor growth and <i>PD-L1</i> expression. In conclusion, <i>TUG1</i> promotes HCC progression by enhancing <i>PD-L1</i> through miR-377-3p, with its knockdown enhancing the therapeutic efficacy of LEN, highlighting <i>TUG1</i>’s potential as a novel target for HCC treatment.</p>

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TUG1 targeting enhances anticancer immunity thereby facilitating lenvatinib efficacy in hepatocellular carcinoma

  • 期刊论文

  • 发表日期：

    2025年9月15日

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  • Siyao Che,
  • Longguang He,
  • Qinshou Chen,
  • Yiqiao Mo,
  • Fuliang Li,
  • Junwei Huang,
  • Zikang Ruan

摘要

Hepatocellular carcinoma (HCC) is a major cause of cancer death globally, with a poor prognosis. The long non-coding RNA TUG1 has been implicated, but its specific role in HCC remains unclear. RT-qPCR was used to evaluate TUG1 and PD-L1 expression, while GEO and TCGA databases were utilized to compare TUG1 levels between HCC patients and healthy controls. In vitro, including CCK8, colony formation, and transwell, assessed cell growth. CD8 + T cell cytotoxicity was evaluated through HCC cells co-culture experiments, and the interaction of miR-377-3p with TUG1 and PD-L1 was examined using dual-luciferase reporter assays. Results indicated that TUG1 was upregulated in HCC, particularly in advanced-stage disease, and PD-L1 expression positively correlated with TUG1 levels. Notably, lenvatinib (LEN) treatment downregulated both TUG1 and PD-L1 in HCC cells, enhancing CD8 + T cell-mediated cytotoxicity. Overexpression of TUG1 diminished the efficacy of LEN, while TUG1 knockdown enhanced it. Mechanistically, TUG1 was found to sponge miR-377-3p, thereby increasing PD-L1 expression. In vivo, TUG1 knockdown combined with LEN treatment significantly reduced tumor growth and PD-L1 expression. In conclusion, TUG1 promotes HCC progression by enhancing PD-L1 through miR-377-3p, with its knockdown enhancing the therapeutic efficacy of LEN, highlighting TUG1’s potential as a novel target for HCC treatment.