2014
DOI: 10.1155/2014/165303
|View full text |Cite
|
Sign up to set email alerts
|

Decitabine and SAHA-Induced Apoptosis Is Accompanied by Survivin Downregulation and Potentiated by ATRA in p53-Deficient Cells

Abstract: While p53-dependent apoptosis is triggered by combination of methyltransferase inhibitor decitabine (DAC) and histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) in leukemic cell line CML-T1, reactive oxygen species (ROS) generation as well as survivin and Bcl-2 deregulation participated in DAC + SAHA-induced apoptosis in p53-deficient HL-60 cell line. Moreover, decrease of survivin expression level is accompanied by its delocalization from centromere-related position in mitotic cells suggesti… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

1
6
0

Year Published

2016
2016
2023
2023

Publication Types

Select...
6

Relationship

1
5

Authors

Journals

citations
Cited by 6 publications
(7 citation statements)
references
References 51 publications
1
6
0
Order By: Relevance
“…Accordingly, in this study, the effect of HAs on cell cycle and proteins involved in the cell cycle regulation in human promyelocytic leukemia (HL‐60) cell line was investigated. The HL‐60, which lack of p53 expression was attributed to p53 gene deletion (Wolf and Rotter, ), can be induced to undergo apoptosis following chemicals or radiation treatments (Brodska et al, ; Han et al, ). The tumor suppressor p53 is also the key protein in checkpoint pathways, which activation may lead to growth arrest at both G1 and G2/M phases in several cancer cells (Stark and Taylor, ).…”
Section: Discussionmentioning
confidence: 99%
“…Accordingly, in this study, the effect of HAs on cell cycle and proteins involved in the cell cycle regulation in human promyelocytic leukemia (HL‐60) cell line was investigated. The HL‐60, which lack of p53 expression was attributed to p53 gene deletion (Wolf and Rotter, ), can be induced to undergo apoptosis following chemicals or radiation treatments (Brodska et al, ; Han et al, ). The tumor suppressor p53 is also the key protein in checkpoint pathways, which activation may lead to growth arrest at both G1 and G2/M phases in several cancer cells (Stark and Taylor, ).…”
Section: Discussionmentioning
confidence: 99%
“…In addition, survivin has been shown to regulate the synthesis of microRNA in human leukocytes by limiting the expression of microRNA biosynthesis-controlling proteins at a posttranscriptional level [29]. Most types of cancer are characterized by overexpression of BIRC5 [30]; they include the following types of cancer: breast, liver, ovarian, bladder, lung, stomach, and esophageal and hematological malignancies. In cancer cells, survivin has two main functions; first, it regulates mitosis by forming a CPC complex, and second, it inhibits the process of tumor cell apoptosis.…”
Section: Introductionmentioning
confidence: 99%
“…This gene has two basic functions: cell death regulation and mitosis progression control. As in the case of the previously discussed genes, increased BIRC5 overexpression characterizes most types of cancers [43]. The last four most upregulated genes were PRC1 (protein regulator of cytokinesis 1), DLGAP5 (DLG-associated protein 5), GAS6 (growth arrest specific 6), and NDRG1 (N-myc downstream regulated 1).…”
Section: Discussionmentioning
confidence: 60%