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Updated: Jul 24, 2025

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SDPR Inhibits TGF-β Induced Cancer Metastasis Through Fatty Acid Oxidation Regulation in Gastric Cancer

Xiaoyue Li1, Jing Luo2, Kelin Mou1

  • 1Department of Oncology, The Affiliated Hospital of Southwest Medical University, Sichuan, Luzhou, 644000, China.

International Journal of Biological Sciences
|July 7, 2023
PubMed

Insights

Transforming growth factor-β (TGF-β) signaling impacts gastric cancer metastasis. This study reveals serum deprivation protein response (SDPR) is downregulated, inhibiting fatty acid metabolism and offering new therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • Transforming growth factor-β (TGF-β) is implicated in tumor metastasis.
  • Serum deprivation protein response (SDPR) is a potential TGF-β target, but its role in gastric cancer is unknown.

Purpose of the Study:

  • To investigate the role and mechanism of SDPR in gastric cancer.
  • To elucidate the involvement of SDPR in TGF-β-mediated tumor metastasis and gastric cancer metabolism.

Main Methods:

  • Gene microarray and bioinformatic analysis.
  • In vivo and in vitro experimental validation.
  • Investigation of protein interactions and pathway analysis (ERK/PPAR).

Main Results:

  • SDPR is significantly downregulated in gastric cancer.
  • SDPR interacts with extracellular signal-regulated kinase (ERK) and suppresses the ERK/PPAR pathway.
  • SDPR inhibits the expression of Carnitine palmitoyl transferase 1A (CPT1A), a key gene in fatty acid metabolism.

Conclusions:

  • The TGF-β/SDPR/CPT1A axis is crucial for fatty acid oxidation in gastric cancer.
  • SDPR dysregulation impacts tumor microenvironment and metabolic reprogramming.
  • Targeting fatty acid metabolism presents a potential therapeutic strategy for gastric cancer metastasis.
Keywords:
CPT1ASDPRTGF-βfatty acid oxidationgastric cancer

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