Suberoylanilide hydroxamic acid induces apoptosis and sub-G1 arrest of 320 HSR colon cancer cells
<p>Abstract</p> <p>Background</p> <p>Histone deacetylases and histone acetyl transferases covalently modify histone proteins, consequentially altering chromatin architecture and gene expression.</p> <p>Methods</p> <p>The effects of suberoylanilid...
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doaj-c388f4f3ae9d445e9300a2b596c976ff2020-11-24T21:44:28ZengBMCJournal of Biomedical Science1021-77701423-01272010-09-011717610.1186/1423-0127-17-76Suberoylanilide hydroxamic acid induces apoptosis and sub-G1 arrest of 320 HSR colon cancer cellsSun Pei-ChangTzao ChingChen Ban-HenLiu Chen-WeiYu Cheng-PingJin Jong-Shiaw<p>Abstract</p> <p>Background</p> <p>Histone deacetylases and histone acetyl transferases covalently modify histone proteins, consequentially altering chromatin architecture and gene expression.</p> <p>Methods</p> <p>The effects of suberoylanilide hydroxamic acid, a HDAC inhibitor, on 320 HSR colon cells were assessed in 320 HSR colon cancer cells.</p> <p>Results</p> <p>Concentration and time-dependent inhibition of 320 HSR cell proliferation was observed. Treatment of 320 HSR cells with 5 μM SAHA for 72 h significantly inhibited their growth by 50% as compared to that of the control. Fluorescence-activated cell sorting analysis demonstrated significant inhibition of cell cycle progression (sub-G1 arrest) and induction of apoptosis upon various SAHA concentrations after 48 h. In addition, the anti-apoptosis proteins, survivin and Bcl-xL, were significantly inhibited by SAHA after 72 h of treatment. Immunocytochemistry analysis revealed that SAHA-resistant cells were positive for cyclin A (85%), ki-67 (100%), p53 (100%), survivin (100%), and p21 (90%) expression. Furthermore, a significant increase cyclin A-, Ki-67-, p53-, survivin-, and p21-positive cells were noted in SAHA-resistant tumor cells.</p> <p>Conclusion</p> <p>Our results demonstrated for the first time in 320 HSR colon adenocarcinoma cells that SAHA might be considered as an adjuvant therapy for colon adenocarcinoma.</p> http://www.jbiomedsci.com/content/17/1/76 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Sun Pei-Chang Tzao Ching Chen Ban-Hen Liu Chen-Wei Yu Cheng-Ping Jin Jong-Shiaw |
spellingShingle |
Sun Pei-Chang Tzao Ching Chen Ban-Hen Liu Chen-Wei Yu Cheng-Ping Jin Jong-Shiaw Suberoylanilide hydroxamic acid induces apoptosis and sub-G1 arrest of 320 HSR colon cancer cells Journal of Biomedical Science |
author_facet |
Sun Pei-Chang Tzao Ching Chen Ban-Hen Liu Chen-Wei Yu Cheng-Ping Jin Jong-Shiaw |
author_sort |
Sun Pei-Chang |
title |
Suberoylanilide hydroxamic acid induces apoptosis and sub-G1 arrest of 320 HSR colon cancer cells |
title_short |
Suberoylanilide hydroxamic acid induces apoptosis and sub-G1 arrest of 320 HSR colon cancer cells |
title_full |
Suberoylanilide hydroxamic acid induces apoptosis and sub-G1 arrest of 320 HSR colon cancer cells |
title_fullStr |
Suberoylanilide hydroxamic acid induces apoptosis and sub-G1 arrest of 320 HSR colon cancer cells |
title_full_unstemmed |
Suberoylanilide hydroxamic acid induces apoptosis and sub-G1 arrest of 320 HSR colon cancer cells |
title_sort |
suberoylanilide hydroxamic acid induces apoptosis and sub-g1 arrest of 320 hsr colon cancer cells |
publisher |
BMC |
series |
Journal of Biomedical Science |
issn |
1021-7770 1423-0127 |
publishDate |
2010-09-01 |
description |
<p>Abstract</p> <p>Background</p> <p>Histone deacetylases and histone acetyl transferases covalently modify histone proteins, consequentially altering chromatin architecture and gene expression.</p> <p>Methods</p> <p>The effects of suberoylanilide hydroxamic acid, a HDAC inhibitor, on 320 HSR colon cells were assessed in 320 HSR colon cancer cells.</p> <p>Results</p> <p>Concentration and time-dependent inhibition of 320 HSR cell proliferation was observed. Treatment of 320 HSR cells with 5 μM SAHA for 72 h significantly inhibited their growth by 50% as compared to that of the control. Fluorescence-activated cell sorting analysis demonstrated significant inhibition of cell cycle progression (sub-G1 arrest) and induction of apoptosis upon various SAHA concentrations after 48 h. In addition, the anti-apoptosis proteins, survivin and Bcl-xL, were significantly inhibited by SAHA after 72 h of treatment. Immunocytochemistry analysis revealed that SAHA-resistant cells were positive for cyclin A (85%), ki-67 (100%), p53 (100%), survivin (100%), and p21 (90%) expression. Furthermore, a significant increase cyclin A-, Ki-67-, p53-, survivin-, and p21-positive cells were noted in SAHA-resistant tumor cells.</p> <p>Conclusion</p> <p>Our results demonstrated for the first time in 320 HSR colon adenocarcinoma cells that SAHA might be considered as an adjuvant therapy for colon adenocarcinoma.</p> |
url |
http://www.jbiomedsci.com/content/17/1/76 |
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