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<p>Cholangiocarcinoma (CCA) is a highly aggressive hepatobiliary malignancy by a poor prognosis. circular RNAs (circRNAs) have poorly characterized roles in CCA. This study identified that circZFX was significantly upregulated in 4 CCA cell lines and 20 paired CCA/normal tissues. circZFX knockdown suppressed CCA proliferation, migration, and invasion in vitro and reduced xenograft tumor volume by 57% in vivo. Mechanistically, circZFX functions as a competing endogenous RNA for miR-654-3p, thus derepressing HDGF. miR-654-3p inhibitor could reverse the inhibitory effects on the proliferation activity, migration, and invasion capabilities of HuCCT1 and QBC939 cells caused by circZFX silencing. Importantly, co-immunoprecipitation revealed HDGF interaction with YAP1, and circZFX knockdown downregulated YAP1 expression. These findings indicate that inhibition of circZFX suppresses malignant phenotypes in cholangiocarcinoma via the miR-654-3p/HDGF and YAP1 signaling activation, highlighting this axis as a novel therapeutic target and providing mechanistic insights for molecular subtyping and the development of circRNA-based precision therapeutics.</p>

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Inhibition of circZFX suppresses malignant phenotypes in cholangiocarcinoma via the miR-654-3p/HDGF and YAP1 signaling activation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月20日

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  • Tingming Liang,
  • Chengxuan Gong,
  • Xinbing Yang,
  • Jie Shen,
  • Guijie Jiang,
  • Jiarui Liu,
  • Guang Yang,
  • Li Guo

摘要

Cholangiocarcinoma (CCA) is a highly aggressive hepatobiliary malignancy by a poor prognosis. circular RNAs (circRNAs) have poorly characterized roles in CCA. This study identified that circZFX was significantly upregulated in 4 CCA cell lines and 20 paired CCA/normal tissues. circZFX knockdown suppressed CCA proliferation, migration, and invasion in vitro and reduced xenograft tumor volume by 57% in vivo. Mechanistically, circZFX functions as a competing endogenous RNA for miR-654-3p, thus derepressing HDGF. miR-654-3p inhibitor could reverse the inhibitory effects on the proliferation activity, migration, and invasion capabilities of HuCCT1 and QBC939 cells caused by circZFX silencing. Importantly, co-immunoprecipitation revealed HDGF interaction with YAP1, and circZFX knockdown downregulated YAP1 expression. These findings indicate that inhibition of circZFX suppresses malignant phenotypes in cholangiocarcinoma via the miR-654-3p/HDGF and YAP1 signaling activation, highlighting this axis as a novel therapeutic target and providing mechanistic insights for molecular subtyping and the development of circRNA-based precision therapeutics.