Actinomycin D induces non-random apoptotic DNA breakpoints in human leukemia HL-60 cells.

Apoptosis is a programmed cell death that is induced by prolonged cellular stress. During apoptosis, caspase-activated DNase cleaves DNA at the internucleosomal regions to produce an “apoptotic ladder” that consists of multiples of 180-200bp. We postulate that these apoptotic DNA breakpoints are non...

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Main Author: Lin, Lifang.
Other Authors: School of Biological Sciences
Format: Final Year Project
Language:English
Published: 2011
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Online Access:http://hdl.handle.net/10356/44275
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Institution: Nanyang Technological University
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spelling sg-ntu-dr.10356-442752023-02-28T18:05:26Z Actinomycin D induces non-random apoptotic DNA breakpoints in human leukemia HL-60 cells. Lin, Lifang. School of Biological Sciences Duke-NUS Medical School Melissa Jane Fullwood DRNTU::Science::Biological sciences::Molecular biology Apoptosis is a programmed cell death that is induced by prolonged cellular stress. During apoptosis, caspase-activated DNase cleaves DNA at the internucleosomal regions to produce an “apoptotic ladder” that consists of multiples of 180-200bp. We postulate that these apoptotic DNA breakpoints are non-random and may be associated with cancer. Previously, our laboratory sequenced the 180-200bp band of the apoptotic ladder DNA of human leukemia HL-60 cells after treating them with actinomycin D for 19 hours. This study aims to validate these results using quantitative PCR at 13 sites near genes and to examine the differences between apopotic breakpoints of HL-60 cells after 4 hours and 19 hours of actinomycin D treatment. Our results showed that actinomycin D-induced apoptosis in HL-60 cells produced specific apoptotic DNA breakpoints, which was consistent with the previous sequencing studies. Some sites of cleavage were near to apoptosis-associated genes (e.g.BIM) and translocated-associated genes (e.g.CREB3L2). In addition, there was no significant difference in the apoptotic breakpoints between 4 hours and 19 hours of actinomycin D-treated HL-60 cells. The discovery of these sites near genes allows us to understand apoptosis in cancer cells better and may provide a platform for further research in cancer treatment. Bachelor of Science in Biological Sciences 2011-05-31T08:01:56Z 2011-05-31T08:01:56Z 2011 2011 Final Year Project (FYP) http://hdl.handle.net/10356/44275 en Nanyang Technological University 37 p. application/pdf
institution Nanyang Technological University
building NTU Library
continent Asia
country Singapore
Singapore
content_provider NTU Library
collection DR-NTU
language English
topic DRNTU::Science::Biological sciences::Molecular biology
spellingShingle DRNTU::Science::Biological sciences::Molecular biology
Lin, Lifang.
Actinomycin D induces non-random apoptotic DNA breakpoints in human leukemia HL-60 cells.
description Apoptosis is a programmed cell death that is induced by prolonged cellular stress. During apoptosis, caspase-activated DNase cleaves DNA at the internucleosomal regions to produce an “apoptotic ladder” that consists of multiples of 180-200bp. We postulate that these apoptotic DNA breakpoints are non-random and may be associated with cancer. Previously, our laboratory sequenced the 180-200bp band of the apoptotic ladder DNA of human leukemia HL-60 cells after treating them with actinomycin D for 19 hours. This study aims to validate these results using quantitative PCR at 13 sites near genes and to examine the differences between apopotic breakpoints of HL-60 cells after 4 hours and 19 hours of actinomycin D treatment. Our results showed that actinomycin D-induced apoptosis in HL-60 cells produced specific apoptotic DNA breakpoints, which was consistent with the previous sequencing studies. Some sites of cleavage were near to apoptosis-associated genes (e.g.BIM) and translocated-associated genes (e.g.CREB3L2). In addition, there was no significant difference in the apoptotic breakpoints between 4 hours and 19 hours of actinomycin D-treated HL-60 cells. The discovery of these sites near genes allows us to understand apoptosis in cancer cells better and may provide a platform for further research in cancer treatment.
author2 School of Biological Sciences
author_facet School of Biological Sciences
Lin, Lifang.
format Final Year Project
author Lin, Lifang.
author_sort Lin, Lifang.
title Actinomycin D induces non-random apoptotic DNA breakpoints in human leukemia HL-60 cells.
title_short Actinomycin D induces non-random apoptotic DNA breakpoints in human leukemia HL-60 cells.
title_full Actinomycin D induces non-random apoptotic DNA breakpoints in human leukemia HL-60 cells.
title_fullStr Actinomycin D induces non-random apoptotic DNA breakpoints in human leukemia HL-60 cells.
title_full_unstemmed Actinomycin D induces non-random apoptotic DNA breakpoints in human leukemia HL-60 cells.
title_sort actinomycin d induces non-random apoptotic dna breakpoints in human leukemia hl-60 cells.
publishDate 2011
url http://hdl.handle.net/10356/44275
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