Decalepis hamiltonii inhibits tumor progression and metastasis by regulating the inflammatory mediators and nuclear factor κB subunits

Integr Cancer Ther. 2014 Mar;13(2):141-51. doi: 10.1177/1534735413502075. Epub 2013 Sep 8.

Abstract

Metastasis is an extremely complex process that is a major problem in the management of cancer. In the present study, we had evaluated the antimetastatic activity of DECALEPIS HAMILTONI: using B16F-10 melanoma-induced experimental lung metastasis in a C57BL/6 mice model.

D hamiltoni: treatment significantly ( : < .01) inhibited lung tumor nodule formation and reduced the lung collagen hydroxyproline, hexosamine, and uronic acid levels. Similarly serum sialic acid and γ-glutamyl transpeptidase levels were also significantly inhibited after

D hamiltoni: treatment. The levels of proinflammatory cytokines such as tumor necrosis factor α, interleukin (IL)-1β, IL-6, granulocyte monocyte colony-stimulating factor, and IL-2 in the serum of these animals were significantly altered after

D hamiltoni: treatment. The serum NO level was also found to be significantly decreased after

D hamiltoni: treatment. This decreased NO level after

D hamiltoni: treatment was also accompanied by decreased inducible NO synthase and cyclooxygenase-2 expression. The study reveals that

D hamiltoni: treatment could alter proinflammatory cytokine production and could inhibit the activation and nuclear translocation of p65 and p50 subunits of nuclear factor κB in B16F-10 cells.

Keywords: Decalepis hamiltonii; metastasis; nuclear factor κB; proinflammatory cytokines.

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cyclooxygenase 2 / metabolism
  • Fabaceae
  • Gene Expression Regulation, Neoplastic / drug effects
  • Granulocyte-Macrophage Colony-Stimulating Factor / metabolism
  • Inflammation / drug therapy*
  • Inflammation / metabolism
  • Lung Neoplasms / drug therapy
  • Male
  • Melanoma, Experimental / drug therapy
  • Mice
  • Mice, Inbred C57BL
  • NF-kappa B / metabolism*
  • Neoplasm Metastasis / drug therapy*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase / metabolism
  • Plant Extracts / pharmacology*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • NF-kappa B
  • Plant Extracts
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • Nitric Oxide Synthase
  • Cyclooxygenase 2