Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

The histone demethylase JMJD1A is essential to prostate cancer cells through regulation of c-Myc expression

ABSTRACT: Analysis of gene expresssion altered upon knockdown of histone demethylase JMJD1A in human prostate cancer cells. The objective is to elucidate the transcriptional programs that are controlled by JMJD1A in human prostate cancer. CWR22Rv1 prostate cancer cells were transduced with lentiviral particles encoding control pLKO.1 or JMJD1A shRNA (shJMJD1A). After 48 h, total RNAs were collected for the microarray analysis to determine the differentially expressed genes between Rv1 pLKO.1 and Rv1 shJMJD1A samples.

ORGANISM(S): Homo sapiens

SUBMITTER: Natasha Sahgal

PROVIDER: E-GEOD-70498 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Publications

Regulation of c-Myc expression by the histone demethylase JMJD1A is essential for prostate cancer cell growth and survival.

Fan L L Peng G G Sahgal N N Fazli L L Gleave M M Zhang Y Y Hussain A A Qi J J

Oncogene 20150817 19

The histone demethylase JMJD1A, which controls gene expression by epigenetic regulation of H3K9 methylation marks, functions in diverse activities, including spermatogenesis, metabolism and stem cell self-renewal and differentiation. Here, we found that JMJD1A knockdown in prostate cancer cells antagonizes their proliferation and survival. Profiling array analyses revealed that JMJD1A-dependent genes function in cellular growth, proliferation and survival, and implicated that the c-Myc transcrip ...[more]

PMID: 26279298

Similar Datasets

Project description:Hypoxia is one of the major driving forces mediating tumor angiogenesis, aggressiveness, as well as resistance to chemo- and radiotherapy. It has also been suggested to play important roles in stem cell maintenance for both normal and cancer tissues. However, the mechanisms by which hypoxia-driven epigenetic changes modulate tumorigenesis remain poorly understood. As the histone H3 lysine 9 (H3K9) demethylase Jmjd1a and methyltransferase G9a are upregulated downstream targets of hypoxia, we focused on these two catalytically opposing epigenetic modifiers to address this question. Through the use of homozygous Jmjd1a and G9a knockout mouse embryonic stem (ES) cells, we found that Jmjd1a was not required for stem cell self-renewal and that anti-angiogenesis related genes were epigenetically dysregulated in both Jmjd1a- and G9a deficient ES cells under hypoxic conditions, accompanied by corresponding changes in H3K9 dimethylation and H3K4 trimethylation levels in the proximal promoter regions of these target genes. Most importantly, these genetic alterations led to opposing tumor phenotypes: loss of Jmjd1a results in increased tumor growth, whereas loss of G9a produces smaller tumors. These findings provide new insights on the importance of hypoxia signalling in regulating the epigenetic status and expression of angiogenesis genes that promote tumor progression. 63 microarray samples consisting of 7 mouse ES cell lines of which 2 are wild type (control), 2 Jmjd1a knockout, 2 G9a knockout and 1 G9a knockout that was reconstituted for G9a (G9a control). Each cell line and condition was seeded at 3 different densities (2X10^5, 4X10^5 and 6X10^5) in 6 cm dishes to control for the effects of cell confluency on gene expression. 18 hours after plating, the cells were subjected to normoxia (21% O2) for 24 hours (control), normoxia 20 hours followed by hypoxia (1% O2) for 4 hours (acute hypoxia) and 24 hours hypoxia (chronic treatment). Total RNA was harvested from all samples for microarrays after the 24 hour treatments.

Dataset Information

The histone demethylase JMJD1A is essential to prostate cancer cells through regulation of c-Myc expression

Publications

Regulation of c-Myc expression by the histone demethylase JMJD1A is essential for prostate cancer cell growth and survival.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets