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Trichostatin A increases radiosensitization of tongue squamous cell carcinoma via miR‑375

Lingfei Jia1, Shan Zhang1, Yiping Huang2

  • 1Central Laboratory, Peking University School and Hospital of Stomatology, Beijing 100081, P.R. China.

Oncology Reports
|November 24, 2016
PubMed

Insights

Trichostatin A (TSA) enhances radiosensitization in tongue squamous cell carcinoma (TSCC) by increasing miR-375 expression. This mechanism involves histone acetylation, leading to apoptosis and potential new therapeutic strategies for TSCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Trichostatin A (TSA), a histone deacetylase inhibitor, shows anti-carcinogenic and radiosensitizing properties.
  • The precise mechanism of TSA's radiosensitization in tongue squamous cell carcinoma (TSCC) is not fully understood.

Purpose of the Study:

  • To investigate the role of TSA in promoting miR-375 expression.
  • To elucidate the effects of TSA and miR-375 on the radiosensitivity of TSCC cells.
  • To explore the underlying molecular mechanisms.

Main Methods:

  • TSA treatment of TSCC cells.
  • Assessment of radiosensitizing effects and apoptosis induction.
  • Analysis of miR-375 expression and its correlation with TSA treatment.
  • Investigation of histone acetylation status at the miR-375 promoter.
  • Measurement of PDK1 and phosphorylated AKT levels.

Main Results:

  • TSA demonstrated significant radiosensitizing effects on TSCC cells.
  • Overexpression of miR-375 mimicked TSA's sensitizing effects, while knockdown attenuated TSA-induced apoptosis.
  • TSA increased histone acetylation of the miR-375 promoter, upregulating miR-375 expression.
  • Upregulated miR-375 led to decreased PDK1 and phosphorylated AKT levels.

Conclusions:

  • TSA enhances radiosensitization and apoptosis in TSCC cells, at least partially through the miR-375 pathway.
  • TSA or miR-375, in combination with radiotherapy, represents a promising therapeutic strategy for TSCC.

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