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...
Saved in:
Main Author: | |
---|---|
Other Authors: | |
Format: | Final Year Project |
Language: | English |
Published: |
2011
|
Subjects: | |
Online Access: | http://hdl.handle.net/10356/44275 |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Institution: | Nanyang Technological University |
Language: | English |
id |
sg-ntu-dr.10356-44275 |
---|---|
record_format |
dspace |
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 |
_version_ |
1759857008155033600 |