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Sodium selenite attenuates lung adenocarcinoma progression by repressing SOX2-mediated stemness

Weiwei Chen1, Jiajia An1, Jiwei Guo1

  • 1Cancer Research Institute, Binzhou Medical University Hospital, No. 661 Huanghe Street, Binzhou, 256600, Shandong, People's Republic of China.

Cancer Chemotherapy and Pharmacology
|March 17, 2018
PubMed
Abstract

Insights

Sodium selenite inhibits lung adenocarcinoma progression by targeting SOX2 and GLI1. This compound shows potential as a therapeutic agent for lung cancer, effectively reducing cancer stemness.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Sodium selenite (SS) is known to induce apoptosis in cancer cells.
  • The precise mechanisms of SS in suppressing lung cancer stem cells are not fully understood.

Purpose of the Study:

  • To investigate the molecular mechanisms of SS in repressing lung adenocarcinoma (LAD) stemness.
  • To evaluate the effects of SS on LAD cells with varying SOX2 expression levels.

Main Methods:

  • In vitro assays assessed cell proliferation, apoptosis, migration, and sphere formation.
  • SOX2 and GLI1 expression levels were analyzed in LAD cells treated with SS.
  • Experiments included LAD cells with and without SOX2 overexpression.

Main Results:

  • SS inhibited LAD cell growth and induced apoptosis in a dose-dependent manner.
  • SS significantly repressed SOX2 and GLI1 expression, reducing stemness.
  • Overexpression of SOX2 partially reversed the anti-cancer effects of SS.

Conclusions:

  • SS attenuates lung adenocarcinoma progression by inhibiting the SOX2/GLI1 pathway.
  • SS demonstrates potential as a therapeutic drug candidate for lung cancer.
Keywords:
CSCsHedgehogLung adenocarcinoma (LAD)SOX2Sodium selenite (SS)

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