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Autophagy Deficiency Induced by SAT1 Potentiates Tumor Progression in Triple-Negative Breast Cancer

Wenwen Tian1,2, Lewei Zhu3, Yongzhou Luo1

  • 1State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, P. R. China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|July 29, 2024
PubMed

Insights

Spermidine/Spermine N1-acetyltransferase 1 (SAT1) drives aggressive triple-negative breast cancer (TNBC) progression. Targeting the SAT1/YBX1/mTOR pathway may offer a new therapeutic strategy for TNBC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Triple-negative breast cancer (TNBC) lacks targeted therapies.
  • The role of Spermidine/Spermine N1-acetyltransferase 1 (SAT1) in TNBC requires further investigation.

Purpose of the Study:

  • To elucidate the role and mechanism of SAT1 in TNBC progression.
  • To identify SAT1 as a potential therapeutic target for TNBC.

Main Methods:

  • Analysis of SAT1 expression in TNBC patient data.
  • In vitro and in vivo experiments involving SAT1 knockdown in TNBC cells.
  • Investigation of molecular mechanisms including transcription factor binding, protein interactions, and post-translational modifications.

Main Results:

  • High SAT1 expression correlates with poor prognosis in TNBC patients.
  • SAT1 knockdown inhibits TNBC cell proliferation and migration.
  • JUN transcription factor upregulates SAT1.
  • SAT1 stabilizes YBX1 protein via deubiquitylation mediated by HERC5.
  • SAT1 suppresses autophagy by stabilizing mTOR mRNA through YBX1-mediated m5C modification.

Conclusions:

  • The SAT1/YBX1/mTOR axis is a key driver of TNBC progression.
  • SAT1 represents a promising therapeutic target for advanced TNBC.
Keywords:
SAT1YBX1autophagym5Ctriple‐negative breast cancer

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