The dual role of autophagy in colorectal cancer

Authors

  • Julia Wojtowicz Student of the Department of Biomedical Sciences, Faculty of Medicine, Medical University of Lodz
  • Zuzanna Senkowska Student of the Department of Biomedical Sciences, Faculty of Medicine, Medical University of Lodz
  • Karolina Niewinna Department of Biochemistry, Institute of Biochemistry and Chemistry, Faculty of Medicine, Medical University of Lodz
  • Urszula Lewandowska Department of Biochemistry, Institute of Biochemistry and Chemistry, Faculty of Medicine, Medical University of Lodz
  • Katarzyna Owczarek Department of Biochemistry, Institute of Biochemistry and Chemistry, Faculty of Medicine, Medical University of Lodz

DOI:

https://doi.org/10.18388/pb.2021_617

Abstract

In recent years, increasing attention has been devoted to cellular processes that modulate tumor progression, particularly autophagy. Current studies indicate a dual role of autophagy in the pathogenesis of colorectal cancer. In the early stages, autophagy serves a protective function by degrading damaged organelles and proteins, whereas in advanced stages, it promotes cancer cell survival. The regulation of autophagy primarily involves the PI3K/Akt/mTOR and AMPK/mTOR signalling pathways, as well as the Beclin-1/PI3K complex. Autophagy-related proteins such as LC3, p62/SQSTM1, and Beclin-1 hold significant diagnostic and prognostic value. Given the impact of autophagy on the efficacy of chemotherapy and targeted therapies, pharmacological modulation of this process has garnered increasing interest. Natural compounds, particularly polyphenols, demonstrate promising multitargeted effects on autophagy. This review comprehensively analyses the molecular mechanisms underlying autophagy in colorectal cancer and evaluates its potential as a therapeutic target. 

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Published

2025-10-01

Issue

Section

Articles