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<p>Existing studies reported that Long non-coding RNA (lncRNA) modulates the stemness of CSCs. Here, we found that LncRNA DBH-antisense RNA 1(AS1) is upregulated in liver CSCs. Forced LncRNA DBH-AS1 promotes tumorigenesis and liver CSCs self-renewal. On the other hand, LncRNA DBH-AS1 expression knockdown prevents liver CSCs from self-renewing. Mechanistically, LncRNA DBH-AS1 mediated regulation of SRY-box transcription factor 4 (SOX4), acting as a ceRNA to sponge miR-612 in liver CSCs. LncRNA DBH-AS1 enhanced liver CSCs self-renew and tumorigenesis via upregulating SOX4. Furthermore, liver cells with LncRNA DBH-AS1 knockdown are susceptible to apoptosis caused by Lenvatinib. Furthermore, the sensitivity of HCC cells with LncRNA DBH-AS1 knockdown to lenvatinib-induced cell death could be reversed by adding SOX4. In conclusion, experimental evidence revealed that METTL3-dependent m<sup>6</sup>A methylation was the mechanism mediating the elevated lncRNADBH-AS1 in HCC. This study demonstrated the critical role that LncRNA DBH-AS1 plays in the carcinogenesis and self-renewal of liver CSCs, which renders it the perfect target for HCC therapy.</p>

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LncRNA DBH-antisense RNA 1 modulates the miR-612/SOX4 axis as a CeRNA to regulate the properties of liver cancer stem cells and their resistance to lenvatinib

  • 期刊论文

  • 发表日期：

    2025年4月5日

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  • Guang-zhen Wu,
  • Yang Liu,
  • Yi-wei Ren,
  • Ting-ting Fan,
  • Teng Zhao,
  • Zhi-ping Huang,
  • Kai Lu

摘要

Existing studies reported that Long non-coding RNA (lncRNA) modulates the stemness of CSCs. Here, we found that LncRNA DBH-antisense RNA 1(AS1) is upregulated in liver CSCs. Forced LncRNA DBH-AS1 promotes tumorigenesis and liver CSCs self-renewal. On the other hand, LncRNA DBH-AS1 expression knockdown prevents liver CSCs from self-renewing. Mechanistically, LncRNA DBH-AS1 mediated regulation of SRY-box transcription factor 4 (SOX4), acting as a ceRNA to sponge miR-612 in liver CSCs. LncRNA DBH-AS1 enhanced liver CSCs self-renew and tumorigenesis via upregulating SOX4. Furthermore, liver cells with LncRNA DBH-AS1 knockdown are susceptible to apoptosis caused by Lenvatinib. Furthermore, the sensitivity of HCC cells with LncRNA DBH-AS1 knockdown to lenvatinib-induced cell death could be reversed by adding SOX4. In conclusion, experimental evidence revealed that METTL3-dependent m6A methylation was the mechanism mediating the elevated lncRNADBH-AS1 in HCC. This study demonstrated the critical role that LncRNA DBH-AS1 plays in the carcinogenesis and self-renewal of liver CSCs, which renders it the perfect target for HCC therapy.