β-Hydroxy-β-methylbutyrate Suppresses NF-ĸB Activation and IL-6 Production in TE-1 Cancer Cells

In Vivo. 2019 Mar-Apr;33(2):353-358. doi: 10.21873/invivo.11481.

Abstract

Background/aim: Stress reactions, especially those related to surgery, cause poor convalescence of cancer patients. β-Hydroxyβ-methylbutyrate (HMB) is known to regulate excessive inflammation in the body. The objective of this work was to investigate the capacity of HMB to suppress activation of nuclear factor-kappa B (NF-ĸB) and production of interleukin-6 (IL-6) in a human esophageal squamous cell carcinoma cell line (TE-1).

Materials and methods: Cell proliferation was measured using the water-soluble tetrazolium-1 method, while tumor necrosis factor alpha (TNFα)-induced IL-6 production was measured using an enzyme-linked immunosorbent assay (ELISA) assay. Nuclear translocation of NF-ĸB was detected by immunofluorescence staining.

Results: HMB did not affect cell proliferation. However, HMB suppressed the TNFα-induced increase in IL-6 production in TE-1 cells by inhibiting NF-ĸB activation.

Conclusion: HMB did not influence TE-1 cell proliferation, but inhibited activation of NF-ĸB and IL-6 production. This result may be useful for improving excessive stress reactions during and after surgery.

Keywords: NF-ĸB; TE-1 cells; β-Hydroxy-β-Methylbutyrate (HMB).

MeSH terms

  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Esophageal Neoplasms / drug therapy*
  • Esophageal Neoplasms / genetics
  • Esophageal Neoplasms / pathology
  • Esophageal Squamous Cell Carcinoma / drug therapy*
  • Esophageal Squamous Cell Carcinoma / genetics
  • Esophageal Squamous Cell Carcinoma / pathology
  • Gene Expression Regulation, Neoplastic / genetics
  • Humans
  • Interleukin-6 / genetics*
  • NF-kappa B / genetics
  • Tumor Necrosis Factor-alpha / genetics
  • Valerates / pharmacology*

Substances

  • Interleukin-6
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Valerates
  • beta-hydroxyisovaleric acid