The Molecular Mechanisms Of Rapamycininduced Autophagy And Apoptosis In T-47d Breast Carcinoma Cells

Autophagy is an evolutionarily conserved lysosomal degradation pathway that leads to degradation of proteins and entire organelles and subsequently plays a crucial role in the homeostatic process of recycling proteins and organelles. Autophagy is an important biological mechanism that enables cel...

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Main Author: Moad, Ahmed Ismail Hassan
Format: Thesis
Language:English
Published: 2013
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Online Access:http://eprints.usm.my/43219/1/Ahmed%20Ismail%20Hassan%20Moad24.pdf
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spelling my-usm-ep.432192019-04-12T05:26:17Z The Molecular Mechanisms Of Rapamycininduced Autophagy And Apoptosis In T-47d Breast Carcinoma Cells 2013-04 Moad, Ahmed Ismail Hassan RK1-715 Dentistry Autophagy is an evolutionarily conserved lysosomal degradation pathway that leads to degradation of proteins and entire organelles and subsequently plays a crucial role in the homeostatic process of recycling proteins and organelles. Autophagy is an important biological mechanism that enables cell survival and to induce death of damage cells. There is increasing evidence that autophagy progresses to autophagic cell death when the process is over-stimulated. Functional relationships have been described between apoptosis (Type I cell death) and autophagic cell death (Type II cell death). However, the molecular relationships and the circumstances of which molecular pathways dictate the choice between autophagy and apoptosis are currently unknown. Autophagy is regulated by the mammalian target of rapamycin (mTOR) kinase pathway. The mTOR are known to inhibit the autophagy process and subsequently lead to tumor development. As a strategy, rapamycin, a known inhibitor of mTOR, was used as an autophagy inducer and 3-methyladenine (3MA) as a classical inhibitor of autophagy. In the present study, a systematic global gene expression was investigated in rapamycin-induced autophagy and the effects of rapamycin when autophagy process is inhibited. The findings have demonstrated that rapamycin was capable of inducing autophagy in T-47D breast carcinoma cells. However, when autophagy was inhibited by 3MA, rapamycin appeared to induce apoptosis in these breast cells. 2013-04 Thesis http://eprints.usm.my/43219/ http://eprints.usm.my/43219/1/Ahmed%20Ismail%20Hassan%20Moad24.pdf application/pdf en public phd doctoral Universiti Sains Malaysia Institut Perubatan & Pergigian Termaju
institution Universiti Sains Malaysia
collection USM Institutional Repository
language English
topic RK1-715 Dentistry
spellingShingle RK1-715 Dentistry
Moad, Ahmed Ismail Hassan
The Molecular Mechanisms Of Rapamycininduced Autophagy And Apoptosis In T-47d Breast Carcinoma Cells
description Autophagy is an evolutionarily conserved lysosomal degradation pathway that leads to degradation of proteins and entire organelles and subsequently plays a crucial role in the homeostatic process of recycling proteins and organelles. Autophagy is an important biological mechanism that enables cell survival and to induce death of damage cells. There is increasing evidence that autophagy progresses to autophagic cell death when the process is over-stimulated. Functional relationships have been described between apoptosis (Type I cell death) and autophagic cell death (Type II cell death). However, the molecular relationships and the circumstances of which molecular pathways dictate the choice between autophagy and apoptosis are currently unknown. Autophagy is regulated by the mammalian target of rapamycin (mTOR) kinase pathway. The mTOR are known to inhibit the autophagy process and subsequently lead to tumor development. As a strategy, rapamycin, a known inhibitor of mTOR, was used as an autophagy inducer and 3-methyladenine (3MA) as a classical inhibitor of autophagy. In the present study, a systematic global gene expression was investigated in rapamycin-induced autophagy and the effects of rapamycin when autophagy process is inhibited. The findings have demonstrated that rapamycin was capable of inducing autophagy in T-47D breast carcinoma cells. However, when autophagy was inhibited by 3MA, rapamycin appeared to induce apoptosis in these breast cells.
format Thesis
qualification_name Doctor of Philosophy (PhD.)
qualification_level Doctorate
author Moad, Ahmed Ismail Hassan
author_facet Moad, Ahmed Ismail Hassan
author_sort Moad, Ahmed Ismail Hassan
title The Molecular Mechanisms Of Rapamycininduced Autophagy And Apoptosis In T-47d Breast Carcinoma Cells
title_short The Molecular Mechanisms Of Rapamycininduced Autophagy And Apoptosis In T-47d Breast Carcinoma Cells
title_full The Molecular Mechanisms Of Rapamycininduced Autophagy And Apoptosis In T-47d Breast Carcinoma Cells
title_fullStr The Molecular Mechanisms Of Rapamycininduced Autophagy And Apoptosis In T-47d Breast Carcinoma Cells
title_full_unstemmed The Molecular Mechanisms Of Rapamycininduced Autophagy And Apoptosis In T-47d Breast Carcinoma Cells
title_sort molecular mechanisms of rapamycininduced autophagy and apoptosis in t-47d breast carcinoma cells
granting_institution Universiti Sains Malaysia
granting_department Institut Perubatan & Pergigian Termaju
publishDate 2013
url http://eprints.usm.my/43219/1/Ahmed%20Ismail%20Hassan%20Moad24.pdf
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