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TRIM44 facilitates ovarian cancer proliferation, migration, and invasion by inhibiting FRK

Xiu-Zhang Yu1,2, Jia-Ling Yuan1,2, Hui Ye1,2

  • 1Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, China.

Neoplasma
|May 26, 2021
PubMed

Insights

TRIM44 promotes ovarian cancer (OC) progression by inhibiting FRK. Reducing TRIM44 expression curbed OC cell proliferation, migration, and invasion, offering new therapeutic insights for this deadly gynecologic cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gynecologic Cancers

Background:

  • Ovarian cancer (OC) is a leading cause of cancer death globally.
  • The role of TRIM44 in OC development and its underlying mechanisms require further investigation.
  • Previous studies suggest TRIM44 plays a role in cancer development.

Purpose of the Study:

  • To investigate the expression of TRIM44 and FRK in OC.
  • To elucidate the functional role of TRIM44 in OC cell proliferation, migration, and invasion.
  • To explore the mechanism by which TRIM44 influences OC progression, specifically its relationship with FRK.

Main Methods:

  • Western blot and RT-qPCR for gene expression analysis.
  • In vitro assays including colony formation, MTT, Transwell, and wound-healing assays.
  • CHIP assay and in vivo xenograft models in mice.

Main Results:

  • TRIM44 was highly expressed, while FRK showed low expression in OC tissues and cell lines.
  • Knocking down TRIM44 significantly inhibited OC cell proliferation, migration, and invasion.
  • FRK was identified as a direct target of TRIM44, with TRIM44 promoting OC progression by inhibiting FRK.

Conclusions:

  • TRIM44 facilitates OC proliferation, migration, and invasion by suppressing FRK expression.
  • TRIM44 acts as a potential oncogene in ovarian cancer.
  • These findings provide novel insights for OC research and therapeutic strategies.

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