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Updated: May 14, 2026

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Published on: March 5, 2018

TRIM16 overexpression induces apoptosis through activation of caspase-2 in cancer cells

Patrick Y Kim1, Aldwin Suryo Rahmanto, Owen Tan

  • 1Children's Cancer Institute Australia for Medical Research, Randwick, NSW 2031, Australia.

Apoptosis : an International Journal on Programmed Cell Death
|February 14, 2013
PubMed

Insights

The tumor suppressor TRIM16 (tripartite motif-containing protein 16) induces apoptosis in cancer cells by directly interacting with and activating caspase-2. This finding reveals a new mechanism for TRIM16

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Tripartite motif-containing protein 16 (TRIM16) functions as a tumor suppressor.
  • TRIM16 interacts with vimentin and E2F1, reducing cancer cell migration and replication.
  • TRIM16 induces apoptosis in breast and lung cancer cells via unknown mechanisms.

Purpose of the Study:

  • To elucidate the mechanism by which TRIM16 induces apoptosis.
  • To investigate the role of TRIM16 in cancer cell apoptosis.

Main Methods:

  • Overexpression of TRIM16 in human breast cancer (MCF7) and neuroblastoma (BE(2)-C) cells.
  • Analysis of caspase-2 protein levels and activity.
  • Co-immunoprecipitation and co-localization studies to assess TRIM16 and caspase-2 interaction.

Main Results:

  • TRIM16 overexpression induced apoptosis in MCF7 and BE(2)-C cells, but not in HEK293 cells.
  • TRIM16 increased procaspase-2 levels and caspase-2 activity in cancer cells.
  • TRIM16 directly interacts with and co-localizes with caspase-2.
  • Caspase-2 activation is essential for TRIM16-induced apoptosis.

Conclusions:

  • TRIM16 promotes apoptosis by directly modulating caspase-2 activity.
  • This study identifies a novel TRIM16-caspase-2 pathway in cancer cell apoptosis.
  • TRIM16's tumor suppressor function is mediated, in part, by caspase-2 activation.

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