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HDAC7 inhibits cell proliferation via NudCD1/GGH axis in triple-negative breast cancer

Mengdi Zhu1,2, Nianqiu Liu1,2,3, Jinna Lin1,2

  • 1Breast Tumor Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, Guangdong 510120, P.R. China.

Oncology Letters
|January 2, 2023
PubMed

Insights

Histone deacetylase 7 (HDAC7) is downregulated in triple-negative breast cancer (TNBC), impacting patient survival. Targeting the HDAC7-NudC domain containing 1 (NudCD1)/γ-glutamyl hydrolase (GGH) axis may offer new therapeutic strategies for TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) lacks effective molecular markers and therapeutic targets.
  • Histone deacetylases (HDACs) regulate gene expression and chromatin remodeling, potentially influencing cancer development.
  • The specific role of HDACs in TNBC treatment remains largely unexplored.

Purpose of the Study:

  • To investigate the expression and prognostic significance of HDAC family members in TNBC.
  • To elucidate the functional role of HDAC7 in TNBC proliferation and its association with key regulatory molecules.
  • To explore the potential of the HDAC7-NudCD1/GGH axis as a therapeutic target for TNBC.

Main Methods:

  • Analysis of HDAC gene expression and prognostic value in TNBC using TCGA and METABRIC databases.
  • In vitro experiments involving HDAC7 silencing and overexpression in TNBC cell lines.
  • Assessment of the association between HDAC7, NudC domain containing 1 (NudCD1), and γ-glutamyl hydrolase (GGH) expression.
  • Evaluation of the impact of the HDAC7-NudCD1/GGH axis on NK cell infiltration.

Main Results:

  • HDAC7 was found to be downregulated in TNBC, with lower expression correlating with shorter patient survival.
  • HDAC7 negatively regulated the expression of NudCD1 and GGH.
  • Silencing HDAC7 increased TNBC cell proliferation, while its overexpression inhibited it.
  • Decreased expression of NudCD1 or GGH also inhibited TNBC cell proliferation.
  • The HDAC7-NudCD1/GGH axis showed an association with NK cell infiltration.

Conclusions:

  • HDAC7 plays a crucial role in regulating TNBC cell proliferation through the NudCD1/GGH pathway.
  • The identified HDAC7-NudCD1/GGH axis represents a novel regulatory mechanism in TNBC.
  • This axis holds promise as a potential therapeutic target for improving TNBC treatment strategies.
Keywords:
NudC domain containing 1histone deacetylase 7triple negative breast cancerγ-glutamyl hydrolase

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