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Correspondence on ‘Role of AMPK/mTOR-independent autophagy in clear cell renal cell carcinoma’ by Radovanovic et al
  1. Shahrokh Lorzadeh1,
  2. Saeid Ghavami2,3,4
  1. 1 Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, Manitoba, Canada
  2. 2 University of Manitoba College of Medicine, Winnipeg, Manitoba, Canada
  3. 3 Research Institute of Oncology and Hematology, Cancer Care Manitoba-University of Manitoba, Winnipeg, Manitoba, Canada
  4. 4 Biology of Breathing Theme, Children Hospital Research Institute of Manitoba, University of Manitoba, Winnipeg, Manitoba, Canada
  1. Correspondence to Professor Saeid Ghavami, Department of Human Anatomy and Cell Sciecne, University of Manitoba College of Medicine, Winnipeg, MB R3E 0J9, Canada; saeid.ghavami{at}

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Dear Editor,

We have read this article published in the Journal of Investigative Medicine with great interest. In this paper, Radovanovic et al 1 investigated macroautophagy (hereafter autophagy) and apoptosis focusing on the regulatory roles of 5'-adenosine monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR) in clear cell renal cell carcinoma (ccRCC). They showed autophagy induction (uncoordinated protein 51-like kinase 1 (ULK1) phosphorylation, LC3 lipidation and p62 degradation) in ccRCC compared with normal renal cells. Interestingly, the active form of AMPK was shown to be lower in ccRCC whereas the phosphorylated form of initiation factor 4E-binding protein 1 (4EBP1), the substrate of mTOR, was increased. Therefore, they concluded that autophagy was executed independent of the AMPK and mTOR pathway.

Autophagy is responsible for degradation and recycling of impaired organelles and cytosolic misfolded proteins to maintain cellular function.2 The autophagy process is executed by autophagy related (ATG) proteins. mTOR is one …

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  • Contributors SL prepared the draft of the manuscript, performed the literature search and prepared the draft figure. SG made the final edit, led and supervised the team and prepared the final manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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