RID: Evaluation of the Possible Inhibiting Effect of the Proinflammatory Signaling Induced by TNF- α through NF- κβ and AP-1 in Two Cell Lines of Breast Cancer

Mediators Inflamm. 2020 Jun 22:2020:2707635. doi: 10.1155/2020/2707635. eCollection 2020.

Abstract

Receptor internalization and degradation (RID), is a transmembrane protein coded within the E3 region expression cassette of adenoviruses. RID downregulates the cell surface expression of epidermal growth factor receptor (EGFR), tumor necrosis factor receptor (TNFR), and apoptosis antigen 1 (FAS), causing a reduction of the effects of their respective ligands. In addition, RID inhibits apoptosis by decreasing the secretion of TNF-related apoptosis-inducing ligand (TRAIL) by normal tissue cells. In this article, we report that RID inhibited chemokine expression in human breast cancer cell line MDA-MB-231 but showed no effect in cell line MCF7. These dissimilar results may be due to the different molecular and functional properties of both cell lines. Therefore, it is necessary to replicate this study in other breast cancer cell models.

MeSH terms

  • Adenoviridae / genetics
  • Adenovirus E3 Proteins / genetics
  • Adenovirus E3 Proteins / physiology*
  • Breast Neoplasms / metabolism*
  • Cell Line, Tumor
  • ErbB Receptors / metabolism
  • Humans
  • MCF-7 Cells
  • Membrane Proteins / genetics
  • Membrane Proteins / physiology*
  • NF-kappa B / metabolism*
  • Receptors, Tumor Necrosis Factor / metabolism
  • Signal Transduction / drug effects
  • Transcription Factor AP-1 / metabolism*
  • Tumor Necrosis Factor-alpha / pharmacology*
  • fas Receptor / metabolism

Substances

  • Adenovirus E3 Proteins
  • E3-13.7 protein, human adenovirus
  • FAS protein, human
  • Membrane Proteins
  • NF-kappa B
  • Receptors, Tumor Necrosis Factor
  • Transcription Factor AP-1
  • Tumor Necrosis Factor-alpha
  • fas Receptor
  • ErbB Receptors