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Protein trafficking in colorectal carcinogenesis-targeting and bypassing resistance to currently applied treatments

Antonios N Gargalionis1, Michalis V Karamouzis1, Christos Adamopoulos1

  • 1Molecular Oncology Unit, Department of Biological Chemistry, University of Athens Medical School, 75M. Asias Street, 11527 Athens, Greece.

Carcinogenesis
|April 12, 2015
PubMed

Insights

Altered protein trafficking in metastatic colorectal cancer (CRC) drives invasion and resistance to targeted therapies. Understanding receptor tyrosine kinase (RTK) transport offers strategies to overcome treatment resistance.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Medicine

Background:

  • Membrane receptors are key targets in metastatic colorectal cancer (CRC) treatment.
  • Aberrant receptor expression/activity promotes cancer cell properties and progression.
  • Protein trafficking ensures correct receptor localization on the cell surface.

Purpose of the Study:

  • To review how protein trafficking influences CRC cell invasion and metastasis.
  • To focus on the endocytic transport of receptor tyrosine kinases (RTKs).
  • To suggest strategies for overcoming RTK-centered resistance mechanisms in CRC.

Main Methods:

  • Literature review of protein trafficking in CRC.
  • Analysis of RTK endocytic transport pathways.
  • Discussion of resistance mechanisms and potential therapeutic strategies.

Main Results:

  • Impaired protein trafficking affects receptor distribution, contributing to defective homeostasis and tumor progression.
  • Dysfunctional trafficking is linked to resistance in CRC-targeted therapy.
  • RTK trafficking plays a critical role in CRC cell invasion and metastasis.

Conclusions:

  • Targeting protein trafficking pathways may offer new therapeutic avenues for CRC.
  • Understanding RTK endocytic transport is crucial for developing strategies against CRC resistance.
  • Modulating protein trafficking could enhance the efficacy of current CRC treatments.

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