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Updated: Dec 15, 2025

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RID: Evaluation of the Possible Inhibiting Effect of the Proinflammatory Signaling Induced by TNF-α through NF-κβ and

F A Monsalve1, A Rojas2, I Gonzalez2

  • 1Department of Basic Biomedical Sciences, Faculty of Health Sciences, University of Talca, Chile.

Mediators of Inflammation
|July 14, 2020
PubMed

Insights

Receptor internalization and degradation (RID) protein affects chemokine expression differently in breast cancer cells. This study found RID inhibited chemokines in MDA-MB-231 cells but not MCF7 cells, suggesting varied cellular responses.

Area of Science:

  • Oncology
  • Molecular Biology
  • Virology

Background:

  • Receptor internalization and degradation (RID) is an adenovirus E3-encoded transmembrane protein.
  • RID modulates cell surface receptor expression, including EGFR, TNFR, and FAS, impacting ligand signaling.
  • RID also influences apoptosis by reducing TRAIL secretion from normal cells.

Purpose of the Study:

  • To investigate the effect of RID on chemokine expression in human breast cancer cell lines.
  • To compare RID's impact on chemokine expression between different breast cancer cell models.

Main Methods:

  • Utilized human breast cancer cell lines MDA-MB-231 and MCF7.
  • Assessed the expression of chemokines in response to RID.

Main Results:

  • RID significantly inhibited chemokine expression in the MDA-MB-231 cell line.
  • No significant effect of RID on chemokine expression was observed in the MCF7 cell line.
  • Differential responses suggest cell-specific molecular and functional properties influence RID activity.

Conclusions:

  • RID exhibits differential effects on chemokine expression in distinct breast cancer cell lines.
  • Further studies using diverse breast cancer models are required to fully elucidate RID's role.
  • Understanding these variations is crucial for exploring RID's therapeutic potential in cancer.

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