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TMED3 promotes prostate cancer via FOXO1a and FOXO3a phosphorylation

Xiuwang Wei1, Jianbo Liang1, Huanwen Huang1

  • 1Department of Urology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530000, China.

Oncology Research
|December 30, 2024
PubMed
Abstract

Insights

Transmembrane emp24 trafficking protein 3 (TMED3) promotes prostate cancer progression by affecting FOXO1a and FOXO3a phosphorylation. Inhibiting TMED3 may offer a new therapeutic strategy for prostate cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Transmembrane emp24 trafficking protein 3 (TMED3) is implicated in various tumors.
  • Its role in prostate cancer progression is not well understood.

Purpose of the Study:

  • To investigate the function of TMED3 in prostate cancer.
  • To elucidate the underlying molecular mechanisms involving the FOXO pathway.

Main Methods:

  • TMED3 was repressed using short hairpin RNA (shRNA) in prostate cancer cells (DU145) and a mouse model.
  • In vitro and in vivo experiments were conducted.
  • Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was performed.

Main Results:

  • TMED3 expression was elevated in prostate cancer cells.
  • TMED3 inhibition reduced proliferation, invasion, and migration, while increasing apoptosis in DU145 cells.
  • TMED3 downregulation suppressed tumor growth, apoptosis, and metastasis in vivo via FOXO1a and FOXO3a phosphorylation.

Conclusions:

  • TMED3 regulates prostate cancer progression through FOXO1a and FOXO3a phosphorylation.
  • TMED3 inhibition presents a potential novel therapeutic strategy for prostate cancer.
Keywords:
ApoptosisProliferationProstate cancerTransmembrane emp24 trafficking protein 3 (TMED3)forkhead box O transcription factor (FOXO)

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