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Autophagy Induction Reduces Telomerase Activity in Hela Cells Publisher Pubmed



Taji F1 ; Kouchesfahani HM1 ; Sheikholeslami F2 ; Romani B3, 4 ; Baesi K5 ; Vahabpour R6 ; Edalati M7 ; Teimooritoolabi L8 ; Jazaeri EO5 ; Abdoli A5
Authors
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Authors Affiliations
  1. 1. Department of Animal Biology, Faculty of Biological Science, Kharazmi University, Tehran, 13169-43551, Iran
  2. 2. WHO Collaborating Center for Reference and Research on Rabies, Pasteur Institute of Iran, Tehran, 13169-43551, Iran
  3. 3. Cellular and Molecular Research Center (CMRC), Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences (AJUMS), Ahvaz, 61357-15794, Iran
  4. 4. Department of Biochemistry, University of Alberta, Edmonton, T6G 2E1, Alberta, Canada
  5. 5. Hepatitis and AIDS Dept., Pasteur Institute of Iran, Tehran, Iran
  6. 6. Medical Lab Technology Department, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  7. 7. Department of Hematology, Allied Medical School, Tehran University of Medical Sciences, Tehran, Iran
  8. 8. Molecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, Iran

Source: Mechanisms of Ageing and Development Published:2017


Abstract

Autophagy is a cellular homeostatic process whereby damaged proteins and organelles are encapsulated into double membrane vesicles, called autophagosomes, for lysosomal digestion. Beclin1 plays a key role in the initial steps of autophagosome formation. In this study, we evaluated the effect of Beclin 1 overexpression in induction of autophagy and the relationship between autophagy induction and telomerase activity in HeLa cells. We found that overexpression of Beclin 1 in HeLa cells leads to autophagosome formation as shown by intracellular autophagosomal marker LC3-II staining. Expression of Beclin1 reduced telomerase activity for about 100 fold compared with the control while it did not affect TERT expression level. The results of cell cycle analysis indicated that the cell cycle and proliferation progressed normally up to 48 h post-transfection. Understanding the role of autophagy induction and telomerase in the pathophysiology of aging and human cancer reveal new strategies that hold much promise for intervention and therapeutic uses. © 2016 Elsevier Ireland Ltd
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