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ORIGINAL ARTICLE
Year : 2021  |  Volume : 17  |  Issue : 1  |  Page : 225-230

Overexpression of Beclin1 gene leads to reduction of telomerase activity in MDCK cells and enhances apoptosis


1 Department of Animal Biology, Faculty of Biological Science, Kharazmi University, Tehran, Iran
2 Department of Hepatitis and AIDS, Pasteur Institute of Iran, Tehran, Iran
3 WHO Collaborating Center for Reference and Research on Rabies, Pasteur Institute of Iran, Tehran, Iran

Correspondence Address:
Homa Mohseni Kouchesfahani
Department of Animal Biology, Faculty of Biological Science, Kharazmi University, Tehran
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcrt.JCRT_265_17

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Background: Telomeres through maintaining chromosomal integrity have key roles in the cell life span. The autophagy is typically a pro-survival process and important for maintaining cellular homeostasis. Conversely, in some conditions, autophagy acts as caspase-independent cell death program. Beclin1 gene plays a principal role in the initiation of autophagy. Objective: The aim of this study was to evaluate the effect of autophagy induction via recombinant Beclin1 on telomerase activity and programmed cell death (apoptosis) in MCDK cells. Materials and Methods: The recombinant Beclin1-pcDNA3.1(-) was transfected into MDCK cells. Next, the autophagy information was detected by LC3II staining as autophagy marker using flow cytometry. The telomerase activity was measured by telomeric repeat amplification protocol method in MDCK cells. To detection of the cell death in MDCK cells, apoptosis assay was done through Annexin V staining method. Results: The results of flow cytometry analysis indicated that following overexpression of Beclin1 gene, the percentage of the LC3II was 16.08% compared with control group (0.48%). Following induction of autophagy, telomerase activity reduced 10 folds in comparison with the control group. The rate of apoptosis in transfected MDCK cells increased up to 12.74%. Conclusion: Crosstalk between telomerase, autophagy, and apoptosis may determine the fate of the cancer cell aging. Hence, manipulation of autophagy may create a novel area to design new compounds and combination therapy to shorten the cancer cell survival.


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