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TRIM56 Suppresses Multiple Myeloma Progression by Activating TLR3/TRIF Signaling

Ying Chen1, Jing Zhao1, Dengzhe Li1

  • 1Department of Hematology, The First Affiliated Hospital of Xi'an Jiao Tong University, Xi'an 710061, China.

Yonsei Medical Journal
|December 8, 2017
PubMed
Abstract

Insights

Tripartite-motif-containing protein 56 (TRIM56) acts as a tumor suppressor in multiple myeloma (MM). Its activation of the TLR3/TRIF pathway inhibits MM cell growth and promotes apoptosis, offering a potential therapeutic strategy.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Tripartite-motif-containing protein 56 (TRIM56) possesses known broad-spectrum antiviral properties linked to its E3 ligase activity.
  • The specific role and molecular mechanisms of TRIM56 in multiple myeloma (MM) pathogenesis remain largely unexplored.

Purpose of the Study:

  • To investigate the functional role of TRIM56 in multiple myeloma (MM).
  • To elucidate the underlying molecular mechanisms by which TRIM56 influences MM cell behavior and the associated signaling pathways.

Main Methods:

  • Quantitative real-time PCR and Western blot were used to assess TRIM56 expression levels in MM cells.
  • Cell proliferation and apoptosis were evaluated using MTT assays and flow cytometry.
  • Interferon-beta (IFN-β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) levels were quantified via ELISA.
  • The impact of TRIM56 on the toll-like receptor 3 (TLR3)/toll-IL-1 receptor (TIR) domain-containing adaptor inducing IFN-β (TRIF) signaling pathway was analyzed by Western blot.

Main Results:

  • TRIM56 expression was significantly reduced in multiple myeloma cells.
  • Overexpression of TRIM56 in U266 cells suppressed proliferation, induced apoptosis, and increased inflammatory cytokine production.
  • Knockdown of TRIM56 in RPMI8226 cells promoted cell growth, reduced apoptosis, and inhibited inflammatory cytokine secretion.
  • TRIM56 knockdown impaired the TLR3 signaling pathway, which was partially restored by TLR3 agonist poly (I:C).

Conclusions:

  • TRIM56 functions as a tumor suppressor in multiple myeloma.
  • The tumor-suppressive activity of TRIM56 is mediated through the activation of the TLR3/TRIF signaling pathway.
  • TRIM56 represents a potential therapeutic target for multiple myeloma treatment.
Keywords:
TLR3/TRIFTRIM56apoptosisinflammatory cytokinemultiple myelomaproliferation

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