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<p>SNAP23 and CPEB4 exhibit promising potential in hepatocellular carcinoma (HCC). This study aimed to investigate their roles in HCC progression and the underlying molecular mechanisms. Using bioinformatics analysis and in vitro experiments in Huh7 cells, we found that SNAP23 was upregulated in HCC and positively correlated with CPEB4. Silencing either gene significantly suppressed cell proliferation and migration while inducing apoptosis. Mechanistically, SNAP23 acted upstream of CPEB4 to regulate autophagy and oxidative stress. Knockdown of SNAP23 or CPEB4 impaired autophagic flux and reduced reactive oxygen species levels. These findings identify SNAP23 and CPEB4 as critical regulators of HCC growth and motility through autophagy‑dependent pathways, highlighting their potential as therapeutic targets.</p>

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SNAP23 regulates CPEB4 in the autophagy of hepatocellular carcinoma

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月5日

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  • Jianzuo Yao,
  • Jingyi Wu,
  • Yaoye Tao,
  • Xie Zhang,
  • Shenzhe Fang,
  • Dansong Yu,
  • Haibiao Wang,
  • Xiaomin Yao,
  • Hong Li

摘要

SNAP23 and CPEB4 exhibit promising potential in hepatocellular carcinoma (HCC). This study aimed to investigate their roles in HCC progression and the underlying molecular mechanisms. Using bioinformatics analysis and in vitro experiments in Huh7 cells, we found that SNAP23 was upregulated in HCC and positively correlated with CPEB4. Silencing either gene significantly suppressed cell proliferation and migration while inducing apoptosis. Mechanistically, SNAP23 acted upstream of CPEB4 to regulate autophagy and oxidative stress. Knockdown of SNAP23 or CPEB4 impaired autophagic flux and reduced reactive oxygen species levels. These findings identify SNAP23 and CPEB4 as critical regulators of HCC growth and motility through autophagy‑dependent pathways, highlighting their potential as therapeutic targets.