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NASP antagonize chromatin accessibility through maintaining histone H3K9me1 in hepatocellular carcinoma

Xuan Kang1, Yun Feng2, Zhixue Gan1

  • 1Research Center for Translational Medicine at East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200092, PR China.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|August 5, 2018
PubMed

Insights

Nuclear autoantigenic sperm protein (NASP) regulates liver cancer by affecting histone deposits. NASP down-regulation inhibits tumor formation and enhances apoptosis, offering cancer prevention insights.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Research

Background:

  • Histone deposition regulation by multi-chaperone complexes is not fully understood.
  • The role of nuclear autoantigenic sperm protein (NASP) in liver cancer requires further investigation.

Purpose of the Study:

  • To investigate the function of NASP in liver cancer regulation.
  • To elucidate the cellular and epigenetic mechanisms underlying NASP's role in liver tumorigenesis.

Main Methods:

  • Analysis of NASP levels in liver tumors versus normal tissues.
  • NASP knockdown in liver cancer cells to assess tumor formation.
  • Investigation of cellular responses and epigenetic modifications (histone H3-H4 shortage, H3K9me1) following NASP depletion.
  • Assessment of gene expression changes (BACH2, RunX1T1, Myc, p53) and apoptosis induction.

Main Results:

  • NASP levels are elevated in liver tumors; NASP down-regulation inhibits tumor growth.
  • NASP knockdown leads to global chromatin accessibility enhancement and replication initiation failure.
  • NASP depletion reduces H3K9me1 modification at anti-tumor gene promoters (BACH2, RunX1T1).
  • Synergistic apoptosis enhancement observed with decreased Myc and p53 levels.

Conclusions:

  • NASP plays a significant role in liver tumorigenesis.
  • NASP down-regulation presents a potential strategy for cancer prevention through epigenetic modulation and apoptosis induction.
Keywords:
H3K9me1Liver cancerNASPReplication stressTranscription

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