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<p>Hepatocellular carcinoma (HCC) is a highly malignant tumor with aggressive progression and poor clinical outcomes, posing a severe threat to global health. Histone deacetylase 7 (HDAC7) has been implicated in the progression of multiple cancers, but the underlying mechanism in HCC cell proliferation remains incomplete. The present study aimed to elucidate the functional contribution of HDAC7 to HCC progression and explore the downstream regulatory network. HDAC7, TRIM26, and CBX4 expression in cells were measured. After silencing HDAC7 expression, HCC cell proliferation was detected. Histone acetylation and HDAC7 enrichment on the TRIM26 promoter were assessed. The binding between TRIM26 and CBX4 was detected. The ubiquitination level of CBX4 was measured. HDAC7 expression was upregulated in HCC cell lines. HDAC7 inhibition suppressed HCC cell proliferation. HDAC7 inhibited TRIM26 expression by mediating histone deacetylation. TRIM26 bound to CBX4 and degraded CBX4 via ubiquitination. Inhibiting TRIM26 or overexpressing CBX4 partially reversed the inhibitory effect of HDAC7 inhibition on HCC cell proliferation. HDAC7 inhibition suppressed the growth of HCC xenografts in vivo. In conclusion, HDAC7 is highly expressed in HCC cells and aggravates malignant proliferation of HCC cells via the TRIM26/CBX4 axis, highlighting HDAC7 as a potential therapeutic target for the development of anti-HCC strategies.</p>

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HDAC7 aggravates malignant proliferation of hepatocellular carcinoma cells via the TRIM26/CBX4 axis

  • 期刊论文

  • 发表日期：

    2026年3月4日

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  • Xinguo Sun,
  • Jianxin Zhang,
  • Qiong Yan,
  • Xiaojun Deng

摘要

Hepatocellular carcinoma (HCC) is a highly malignant tumor with aggressive progression and poor clinical outcomes, posing a severe threat to global health. Histone deacetylase 7 (HDAC7) has been implicated in the progression of multiple cancers, but the underlying mechanism in HCC cell proliferation remains incomplete. The present study aimed to elucidate the functional contribution of HDAC7 to HCC progression and explore the downstream regulatory network. HDAC7, TRIM26, and CBX4 expression in cells were measured. After silencing HDAC7 expression, HCC cell proliferation was detected. Histone acetylation and HDAC7 enrichment on the TRIM26 promoter were assessed. The binding between TRIM26 and CBX4 was detected. The ubiquitination level of CBX4 was measured. HDAC7 expression was upregulated in HCC cell lines. HDAC7 inhibition suppressed HCC cell proliferation. HDAC7 inhibited TRIM26 expression by mediating histone deacetylation. TRIM26 bound to CBX4 and degraded CBX4 via ubiquitination. Inhibiting TRIM26 or overexpressing CBX4 partially reversed the inhibitory effect of HDAC7 inhibition on HCC cell proliferation. HDAC7 inhibition suppressed the growth of HCC xenografts in vivo. In conclusion, HDAC7 is highly expressed in HCC cells and aggravates malignant proliferation of HCC cells via the TRIM26/CBX4 axis, highlighting HDAC7 as a potential therapeutic target for the development of anti-HCC strategies.