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SLC3A2 inhibits ferroptosis in laryngeal carcinoma via mTOR pathway

Fangxing Wu1, Gaoyun Xiong1, Zejun Chen2

  • 1Department of Otolaryngology, Tongde Hospital of Zhejiang Province, No. 234 Gu Chui Road, Hangzhou, Zhejiang Province, China.

Hereditas
|January 21, 2022
PubMed
Abstract

Insights

Solute carrier family 3 member 2 (SLC3A2) negatively regulates ferroptosis in laryngeal carcinoma by suppressing the mTOR pathway. Downregulating SLC3A2 promotes ferroptosis and inhibits tumor growth, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Laryngeal carcinoma is a significant health concern with complex molecular underpinnings.
  • Understanding the mechanisms regulating cell death, such as ferroptosis, is crucial for developing novel therapeutic strategies.
  • The role of specific genes like SLC3A2 in laryngeal carcinoma progression and ferroptosis remains to be fully elucidated.

Purpose of the Study:

  • To investigate the expression of SLC3A2 in laryngeal carcinoma.
  • To explore the functional role of SLC3A2 in regulating ferroptosis in laryngeal carcinoma cells.
  • To elucidate the underlying molecular mechanism involving the mTOR pathway.

Main Methods:

  • Bioinformatic analysis of TCGA data to identify key genes.
  • Stable knockdown of SLC3A2 in laryngeal carcinoma cell lines.
  • Assessment of cell viability, proliferation, and ferroptosis.
  • Analysis of mRNA and protein expression using RT-qPCR and Western blotting.
  • In vivo studies using a xenograft tumor model.

Main Results:

  • SLC3A2 is highly expressed in laryngeal carcinoma tissues and cells, correlating with poor patient survival.
  • Knockdown of SLC3A2 inhibited cell proliferation, foci formation, and tumor growth in vivo.
  • SLC3A2 deficiency induced ferroptosis and suppressed ferroptosis-related protein expression.
  • Mechanistically, SLC3A2 deficiency upregulated mTOR and P70S6K while inhibiting p-mTOR and p-P70S6K, indicating negative regulation of ferroptosis via the mTOR pathway.

Conclusions:

  • SLC3A2 acts as a negative regulator of ferroptosis in laryngeal carcinoma.
  • The mTOR signaling pathway is implicated in SLC3A2-mediated ferroptosis regulation.
  • Targeting SLC3A2 may represent a promising therapeutic strategy for laryngeal carcinoma.
Keywords:
Cell proliferationFerroptosisLaryngeal carcinomaSLC3A2mTOR

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