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Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
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Selenomethionine suppresses head and neck squamous cell carcinoma progression through TopBP1/ATR and TCAB1 signaling

Bo Zhang1,2, Xiaodong Wei3,4, Jiwu Li5

  • 1Hubei Provincial Key Laboratory of Occurrence and Intervention of Rheumatic Diseases, Hubei Minzu University, Enshi City, Hubei Province, China. zhboss1234@163.com.

Histology and Histopathology
|September 26, 2023
PubMed
Abstract

Insights

L-selenomethionine (SeMet) inhibits head and neck squamous cell carcinoma (HNSCC) cell survival and proliferation while promoting apoptosis. This occurs by modulating the TopBP1/ATR and TCAB1 signaling pathways, suggesting SeMet as a potential HNSCC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Head and neck squamous cell carcinoma (HNSCC) is a prevalent cancer.
  • Selenium compounds, including L-selenomethionine (SeMet), show promise in cancer therapy.
  • Understanding the molecular mechanisms of SeMet in HNSCC is crucial for therapeutic development.

Purpose of the Study:

  • To elucidate the mechanism by which L-selenomethionine (SeMet) exerts its anti-cancer effects in head and neck squamous cell carcinoma (HNSCC).
  • To investigate the role of TopBP1/ATR and TCAB1 signaling pathways in SeMet-mediated HNSCC treatment.

Main Methods:

  • Cell viability and proliferation were assessed using MTT and colony formation assays.
  • Apoptosis was evaluated via TUNEL staining.
  • Gene and protein expression levels were quantified using qRT-PCR and Western blotting, respectively.

Main Results:

  • SeMet significantly reduced HNSCC cell survival and proliferation in a dose- and time-dependent manner.
  • SeMet treatment upregulated TopBP1, ATR, H2AX, p-ATR, and γ-H2AX, while downregulating TCAB1.
  • The effects of SeMet were partially reversed by manipulating TopBP1 and TCAB1 expression, indicating their critical roles in the observed outcomes.

Conclusions:

  • L-selenomethionine (SeMet) effectively inhibits HNSCC proliferation and induces apoptosis.
  • The mechanism involves the modulation of TopBP1/ATR signaling activation and TCAB1 expression.
  • SeMet represents a potential therapeutic agent for head and neck squamous cell carcinoma.

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