The RAGE/multiligand axis: a new actor in tumor biology

Armando Rojas1, Ivan Schneider1, Cristian Lindner1

  • 1Biomedical Research Labs., Universidad Catolica del Maule, Facultad de Medicina, 3605 San Miguel Ave., Talca, Chile.

Bioscience Reports
|June 21, 2022
PubMed

Insights

The receptor for advanced glycation end-products (RAGE) is involved in chronic inflammation and cancer. This review details how RAGE activation promotes tumor growth and spread.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • The receptor for advanced glycation end-products (RAGE) is a transmembrane protein implicated in chronic inflammatory diseases.
  • RAGE binds to various ligands, including damage-associated molecular patterns (DAMPs) like HMGB1 and S100 proteins.
  • Emerging evidence highlights RAGE's significant role in tumor biology.

Purpose of the Study:

  • To review the multifaceted roles of the RAGE axis in cancer development and progression.
  • To elucidate how RAGE activation contributes to tumor growth, immune evasion, and metastasis.
  • To describe RAGE's influence on shaping the tumor microenvironment to support cancer progression.

Main Methods:

  • This review synthesizes existing scientific literature on the RAGE axis in cancer.
  • It analyzes studies investigating RAGE's involvement in tumor growth, immune responses, and metastasis.
  • The review focuses on the functional consequences of RAGE activation in the tumor microenvironment.

Main Results:

  • The RAGE axis is actively involved in key cancer mechanisms, including tumor growth and immune evasion.
  • RAGE activation contributes to cancer cell dissemination and metastasis.
  • RAGE plays a crucial role in creating a tumor-supportive microenvironment.

Conclusions:

  • The RAGE axis is a critical mediator of tumor growth, immune escape, and metastasis.
  • Understanding RAGE signaling is essential for developing novel cancer therapies.
  • Targeting the RAGE pathway holds therapeutic potential for various cancers.