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TRIM52 plays an oncogenic role in ovarian cancer associated with NF-kB pathway

Weihong Yang1,2, Li Liu1,2, Caixia Li1,2

  • 1Department of Gynecology and Obstetrics, Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.

Cell Death & Disease
|September 7, 2018
PubMed

Insights

Tripartite motif 52 (TRIM52) promotes ovarian cancer by activating the NF-kB pathway. Reducing TRIM52 inhibits tumor growth and invasion, suggesting it as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • The tripartite motif (TRIM) family is implicated in cancer development.
  • Understanding TRIM family members' roles is crucial for cancer therapy.

Purpose of the Study:

  • To investigate the role of TRIM52 in ovarian cancer tumorigenesis.
  • To elucidate the molecular mechanisms underlying TRIM52's function in ovarian cancer.

Main Methods:

  • Cell culture experiments (SKOV3, CAOV3, HO8910) with TRIM52 knockdown and overexpression.
  • Western blotting to assess protein expression (phospho-IKKβ, IκBα, P65, caspase-3).
  • In vivo studies using nude mice xenografts.

Main Results:

  • TRIM52 knockdown inhibited ovarian cancer cell invasion, migration, and proliferation, while inducing apoptosis.
  • TRIM52 overexpression yielded opposite effects.
  • TRIM52 modulated the NF-kB pathway, affecting downstream targets like MMP9, Bcl2, IL8, TNFα, and caspase-3.
  • TRIM52 knockdown suppressed tumor growth in vivo.

Conclusions:

  • TRIM52 plays an oncogenic role in ovarian cancer.
  • TRIM52 facilitates ovarian cancer development via the NF-kB signaling pathway.
  • TRIM52 represents a potential therapeutic target for ovarian cancer treatment.

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