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自噬诱导降低了HeLa细胞中的端粒酶活性。

Autophagy induction reduces telomerase activity in HeLa cells.

作者信息

Taji Fatemeh, Kouchesfahani Homa Mohseni, Sheikholeslami Farzaneh, Romani Bizhan, Baesi Kazem, Vahabpour Rouhollah, Edalati Mahdi, Teimoori-Toolabi Ladan, Jazaeri Ehsan Ollah, Abdoli Asghar

机构信息

Department of Animal Biology, Faculty of Biological Science, Kharazmi University, Tehran, 13169-43551, Iran.

WHO Collaborating Center for Reference and Research on Rabies, Pasteur Institute of Iran, Tehran, 13169-43551, Iran.

出版信息

Mech Ageing Dev. 2017 Apr;163:40-45. doi: 10.1016/j.mad.2016.12.011. Epub 2016 Dec 30.

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 48h 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.

摘要

自噬是一种细胞稳态过程,通过该过程,受损的蛋白质和细胞器被包裹在称为自噬体的双膜囊泡中,以便进行溶酶体消化。Beclin1在自噬体形成的初始步骤中起关键作用。在本研究中,我们评估了Beclin 1过表达在诱导自噬中的作用以及自噬诱导与HeLa细胞中端粒酶活性之间的关系。我们发现,HeLa细胞中Beclin 1的过表达导致自噬体形成,如细胞内自噬体标志物LC3-II染色所示。与对照组相比,Beclin1的表达使端粒酶活性降低了约100倍,而它不影响TERT的表达水平。细胞周期分析结果表明,转染后48小时内细胞周期和增殖正常进行。了解自噬诱导和端粒酶在衰老和人类癌症病理生理学中的作用,揭示了具有很大干预和治疗应用前景的新策略。

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