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Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
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TRIM44 is indispensable for glioma cell proliferation and cell cycle progression through AKT/p21/p27 signaling

Xia Zhou1,2, Yadong Yang3,4, Pengcheng Ma5

  • 1Key Laboratory of Tumor Immunological Prevention and Treatment of Yunnan Province, Central Laboratory of Yan'an Hospital, Affiliated to Kunming Medical University, 245 East Ren Ming Road, Kunming, 650051, Yunnan, China.

Journal of Neuro-Oncology
|October 13, 2019
PubMed
Abstract

Insights

TRIM44 is elevated in glioma and drives cancer growth. Inhibiting TRIM44 halts glioma cell proliferation and tumor growth, suggesting TRIM44 as a potential therapeutic target for glioma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Glioma is a lethal brain cancer requiring novel therapeutic targets.
  • The role of TRIM44 in glioma's pathophysiology remains largely undefined.
  • TRIM44 is implicated in the carcinogenesis of other human tumors.

Purpose of the Study:

  • To investigate the pathophysiological significance of TRIM44 in glioma.
  • To determine the role of TRIM44 in glioma cell proliferation, apoptosis, and in vivo tumor growth.
  • To elucidate the molecular mechanism underlying TRIM44's function in glioma.

Main Methods:

  • Quantitative-PCR and Western blot assessed TRIM44 expression in glioma cells.
  • Cell proliferation was evaluated using BrdU incorporation and colony formation assays.
  • Apoptosis was analyzed via Caspase 3 staining and FACS analysis.
  • In vivo tumor growth was studied in a BALB/c nude mouse xenograft model.
  • Western blot analyzed the expression of AKT pathway proteins (p21, p27, AKT).

Main Results:

  • TRIM44 expression was significantly elevated in glioma cells and correlated with poor patient prognosis.
  • TRIM44 knockdown inhibited glioma cell proliferation, migration, and induced cell cycle arrest and apoptosis in vitro.
  • TRIM44 inactivation significantly suppressed tumor growth in a xenograft model.
  • TRIM44 deficiency led to upregulation of p21/p27 and inactivation of the AKT pathway.

Conclusions:

  • TRIM44 expression is associated with the oncogenic potential of glioma.
  • TRIM44 inactivation inhibits glioma progression via the AKT/p21/p27 pathway.
  • Targeting TRIM44 presents a promising therapeutic strategy for glioma treatment.
Keywords:
AKTCell cycleMigrationProliferationTRIM44

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