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Updated: Sep 15, 2025

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Sestrin2 Overexpression Inhibits Proliferation and Epithelial-Mesenchymal Transition and Induces Autophagy Through

Yae-Ji Kim1, Hui-Ju Lee1, Kyung-Hyun Kim1

  • 1Department of Veterinary Medicine & Institute of Veterinary Science, Chungnam National University, Daejeon 34134, Republic of Korea.

Prostate Cancer
|July 15, 2025
PubMed

Insights

Sestrin2 (SESN2) inhibits prostate cancer by promoting autophagy via the AMPK/mTOR pathway. Low SESN2 expression correlates with poor patient survival, suggesting SESN2 as a potential therapeutic target for prostate cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Prostate cancer is a leading male malignancy.
  • Sestrin2 (SESN2) exhibits antitumor properties in various cancers.
  • The role of SESN2 in prostate cancer remains largely unexplored.

Purpose of the Study:

  • To investigate the role and mechanism of Sestrin2 (SESN2) in human prostate cancer.
  • To determine if SESN2 affects prostate cancer cell proliferation, migration, invasion, and autophagy.
  • To elucidate the involvement of the AMPK/mTOR signaling pathway in SESN2-mediated effects.

Main Methods:

  • Bioinformatic analysis of The Cancer Genome Atlas and Gene Expression Profiling Interactive Analysis databases.
  • Prostate cancer cell line (PC3, DU145) manipulation using Sestrin2 overexpression vectors.
  • Assessment of cell viability, proliferation, migration, and invasion.
  • Western blot analysis and immunofluorescence staining for autophagy and signaling pathway markers.
  • Pharmacological inhibition of mTOR using rapamycin.

Main Results:

  • SESN2 expression is downregulated in prostate cancer tissues and cell lines.
  • Low SESN2 expression is associated with reduced patient survival.
  • SESN2 overexpression inhibited prostate cancer cell viability, proliferation, migration, and invasion.
  • SESN2 promoted autophagy, evidenced by increased autophagy-related proteins and LC3-positive cells.
  • SESN2 modulated the AMPK/mTOR pathway, increasing pAMPK and decreasing pmTOR levels.

Conclusions:

  • SESN2 suppresses prostate cancer progression by inducing autophagy.
  • The AMPK/mTOR signaling pathway mediates SESN2's pro-autophagic and anti-cancer effects.
  • SESN2 represents a potential novel therapeutic target for prostate cancer treatment.
Keywords:
SESN2autophagymetastasisproliferationprostate cancer

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