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INMAP, a novel truncated version of POLR3B, represses AP-1 and p53 transcriptional activity

Zhou Yunlei1, Chen Zhe, Lei Yan

  • 1Key Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Sciences, Beijing Normal University, Beijing, 100875, People's Republic of China.

Molecular and Cellular Biochemistry
|November 6, 2012
PubMed

Insights

Interphase nucleus and mitotic apparatus-associated protein (INMAP) is a truncated RNA polymerase III subunit found to be upregulated in human cancers. Overexpression inhibits p53 and AP-1, suggesting roles in tumor development.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • INMAP, a nuclear and mitotic apparatus-associated protein, is crucial for spindle formation and cell-cycle progression.
  • INMAP is a truncated form of the RNA polymerase III subunit B (POLR3B).

Purpose of the Study:

  • To investigate the evolutionary conservation and functional roles of INMAP.
  • To explore the potential link between INMAP and human tumorigenesis.

Main Methods:

  • Comparative sequence analysis to assess evolutionary conservation.
  • Expression analysis in human cancer cell lines.
  • Deletion analysis to identify functional domains.
  • Overexpression studies to evaluate effects on transcriptional activity.

Main Results:

  • INMAP is conserved from prokaryotes to humans and upregulated in various cancer cell lines (HeLa, Bel-7402, HepG2, BGC-823).
  • A specific amino acid region (209-290) is essential for INMAP's nuclear localization.
  • INMAP overexpression dose-dependently inhibits p53 and AP-1 transcriptional activities.

Conclusions:

  • INMAP may contribute to tumorigenesis by modulating p53 and AP-1 pathways.
  • INMAP plays dual roles in coordinating cell division with gene expression and influencing cell fate and proliferation.

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