1. Academic Validation
  2. The receptor for advanced glycation end products: A fuel to pancreatic cancer

The receptor for advanced glycation end products: A fuel to pancreatic cancer

  • Semin Cancer Biol. 2018 Apr;49:37-43. doi: 10.1016/j.semcancer.2017.07.010.
Uzma Shahab 1 Mohd Kaleem Ahmad 2 Abbas Ali Mahdi 2 Mohd Waseem 3 Binish Arif 4 Moinuddin 5 Saheem Ahmad 6
Affiliations

Affiliations

  • 1 Department of Biochemistry, King George Medical University, Lucknow, U.P., India. Electronic address: [email protected].
  • 2 Department of Biochemistry, King George Medical University, Lucknow, U.P., India.
  • 3 Department of Biochemistry, King George Medical University, Lucknow, U.P., India; IIRC-1, Laboratory of Glycation Biology and Metabolic Disorders, Integral University, Lucknow, U.P., India; Department of Biosciences, Integral University, Lucknow, U.P., India.
  • 4 Department of Biochemistry, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India.
  • 5 Department of Biochemistry, J.N. Medical College, A.M.U., Aligarh, U.P., India.
  • 6 IIRC-1, Laboratory of Glycation Biology and Metabolic Disorders, Integral University, Lucknow, U.P., India; Department of Biosciences, Integral University, Lucknow, U.P., India.
Abstract

The receptor for advanced glycation end products (RAGEs) was first illustrated in the year 1992. RAGE is a single-transmembrane and multi-ligand component of the immunoglobulin protein super family. The engagement of RAGE turns out to an establishment of numerous intracellular signalling mechanisms resulting in the progression and perpetuation of many types of Cancer including, the pancreatic Cancer. The present review primarily focuses on the multi-ligand activation of RAGEs leading to the downstream signalling cascade activation. The kick start of the RAGEs activation leads to the several anomalies and includes multiple types of cancers. The RAGE expression correlates well with the survival of pancreatic Cancer cells leading to the myeloid response. RAGEs assist in the tumourogenesis which enhance and thrive to its fullest in the stressed tumour microenvironment. An improved perceptive of its involvement in pancreatic Cancer may offer novel targets for tumour supervision and risk measurement.

Keywords

Hypoxia; Pancreatic cancer; RAGE; Signalling; Tumourigenesis.

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