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Propionate of a microbiota metabolite induces cell apoptosis and cell cycle arrest in lung cancer

  • Kwangkho Kim
  • , Ohman Kwon
  • , Tae Young Ryu
  • , Cho Rok Jung
  • , Janghwan Kim
  • , Jeong Ki Min
  • , Dae Soo Kim
  • , Mi Young Son
  • , Hyun Soo Cho
  • Korea Research Institute of Bioscience and Biotechnology
  • University of Science and Technology UST

Research output: Contribution to journalArticlepeer-review

115 Scopus citations

Abstract

Short-chain fatty acids (SCFAs; butyrate, propionate and acetate) are metabolites derived from the gut microbiota via dietary fiber fermentation. In colon cancer, treatment with SCFAs, mainly butyrate and propionate, suppresses cell proliferation, migration and invasion. Furthermore, although sodium butyrate is known to induce cell apoptosis in lung cancer, the anticancer effects of sodium propionate (SP) on lung cancer are not well understood. In the present study, SP treatment induced cell cycle arrest, especially in the G2/M phase, and cell apoptosis in the H1299 and H1703 lung cancer cell lines. As determined by reverse transcription-quantitative PCR and western blotting, Survivin and p21 expression levels were significantly affected by SP treatment, suggesting that SP treatment suppressed cell proliferation in these lung cancer cell lines. Thus, it was proposed that the SP-mediated regulation of Survivin and p21 in lung cancer may be applicable to lung cancer therapy.

Original languageEnglish
Pages (from-to)1569-1574
Number of pages6
JournalMolecular Medicine Reports
Volume20
Issue number2
DOIs
StatePublished - 2019

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Apoptosis
  • Cell cycle
  • Lung cancer
  • P21
  • Propionate
  • Survivin

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