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<p>Research has identified the dysregulation of circular RNA ZFR (circRNA ZFR) as a key factor in hepatocellular carcinoma (HCC) progression, though its precise molecular mechanisms remain unclear. This study assessed circRNA ZFR expression in clinical samples and HCC cells using qRT-PCR and Fluorescent In Situ Hybridization assays. Cell functions were evaluated through colony formation, transwell, and wound healing assays. circRNA ZFR and miR-96a-5p interaction was investigated using luciferase reporter assays and qRT-PCR, while miR-96a-5p and SLC1A1 interaction was examined using luciferase reporter assays, western blot analysis, and Chromatin Isolation by RNA Purification/Mass Spectrometry (CHIRP/MS). CircRNA ZFR was significantly upregulated in blood, tissue samples and HCC cells compared to their respective normal controls (<i>P</i> &lt; 0.001), and were associated with tumor differentiation (r = 0.249, <i>p</i> = 0.031), tumor size (r = 0.258, <i>p</i> = 0.027) and tumor-node-metastasis (TNM) stage (r = 0.287, <i>p</i> = 0.020). CircRNA ZFR overexpression promoted HCC cell proliferation, migration and invasion while its knockdown inhibited HCC progression. miR-96a-5p was identified as the putative target for CircRNA ZFR and its inhibition promoted HCC through modulating the expression of SLC1A1 gene. Collectively, circRNA ZFR knockdown retarded HCC progression by sponging miR-96a-5p and modulating SLC1A1 expression, suggesting that the circZFR/miR-96a-5p/SLC1A1 axis may serve as potential therapeutic targets for HCC.</p>

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CircRNA ZFR promotes cell progression by regulating miR-96a-5p/SLC1A1 axis in hepatocellular carcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月15日

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  • Christian Cedric Bongolo,
  • Yu Zhang,
  • ShengBao Duan,
  • Louise Virginie Mounoume Lobe,
  • Erick Thokerunga,
  • Peter kisembo,
  • HongMei Wang,
  • ShaoHua Ding,
  • JingJing Tian,
  • YeZhou Chen,
  • YuJue Wang,
  • Liu Jie,
  • YuQin Chao,
  • JianCheng Tu

摘要

Research has identified the dysregulation of circular RNA ZFR (circRNA ZFR) as a key factor in hepatocellular carcinoma (HCC) progression, though its precise molecular mechanisms remain unclear. This study assessed circRNA ZFR expression in clinical samples and HCC cells using qRT-PCR and Fluorescent In Situ Hybridization assays. Cell functions were evaluated through colony formation, transwell, and wound healing assays. circRNA ZFR and miR-96a-5p interaction was investigated using luciferase reporter assays and qRT-PCR, while miR-96a-5p and SLC1A1 interaction was examined using luciferase reporter assays, western blot analysis, and Chromatin Isolation by RNA Purification/Mass Spectrometry (CHIRP/MS). CircRNA ZFR was significantly upregulated in blood, tissue samples and HCC cells compared to their respective normal controls (P < 0.001), and were associated with tumor differentiation (r = 0.249, p = 0.031), tumor size (r = 0.258, p = 0.027) and tumor-node-metastasis (TNM) stage (r = 0.287, p = 0.020). CircRNA ZFR overexpression promoted HCC cell proliferation, migration and invasion while its knockdown inhibited HCC progression. miR-96a-5p was identified as the putative target for CircRNA ZFR and its inhibition promoted HCC through modulating the expression of SLC1A1 gene. Collectively, circRNA ZFR knockdown retarded HCC progression by sponging miR-96a-5p and modulating SLC1A1 expression, suggesting that the circZFR/miR-96a-5p/SLC1A1 axis may serve as potential therapeutic targets for HCC.