Molecular Response of Human Monocytes Following Interaction with Colon Cancer Cells by Pre-treatment with Low-dose Lipopolysaccharide

Anticancer Res. 2015 Aug;35(8):4473-7.

Abstract

Background/aim: The increased mRNA expression of chemotaxis- and angiogenesis-related factors in human monocytes following interaction with colon cancer cells has been shown to be suppressed by pre-treatment with low-dose lipopolysaccharide (LPS) (100 pg/ml). It has been demonstrated that low-dose LPS reduced the expression of RelB, a member of the nuclear factor (NF)-κB transcription factor family, in mouse macrophages and the NF-κB signaling pathway was important for tumor initiation and growth in tumor-associated macrophages. In addition, the signal transducer and activator of transcription 3 (STAT3) regulated innate immunity via Toll-like receptor (TLR)4 signaling. In the present study, the mRNA expression of signaling pathway- and suppression-related genes in human monocytes following a low-dose LPS treatment and subsequent interaction with colon cancer cells was investigated, in order to assess the molecular response.

Materials and methods: The human monocyte cell line THP-1 was treated with LPS and, subsequently, co-cultured with the human colon cancer cell line DLD-1. The mRNA expression of various genes was then analyzed using quantitative real-time polymerase chain reaction (PCR).

Results: The mRNA expression of RelB, STAT3, interleukin (IL)-10 and transforming growth factor (TGF)-β in THP-1 cells following interaction with DLD-1 cells was suppressed by pre-treatment with low-dose LPS (100 pg/ml).

Conclusion: Treating human monocytes with low-dose LPS may be useful for suppressing tumor progression and may be valuable for maintaining homeostasis.

Keywords: RelB; STAT3; co-culture; colon cancer cell; low-dose lipopolysaccharide; monocyte.

MeSH terms

  • Cell Line, Tumor
  • Coculture Techniques
  • Colonic Neoplasms / immunology*
  • Disease Progression*
  • Gene Expression Profiling
  • Humans
  • Interleukin-10 / biosynthesis
  • Lipopolysaccharides / administration & dosage*
  • Macrophages / immunology
  • Monocytes / immunology*
  • RNA, Messenger / biosynthesis
  • STAT3 Transcription Factor / immunology
  • Toll-Like Receptor 4 / immunology
  • Transcription Factor RelB / biosynthesis
  • Transforming Growth Factor beta / biosynthesis

Substances

  • IL10 protein, mouse
  • Lipopolysaccharides
  • RELB protein, human
  • RNA, Messenger
  • STAT3 Transcription Factor
  • Stat3 protein, mouse
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
  • Transforming Growth Factor beta
  • Interleukin-10
  • Transcription Factor RelB