ArticleClinical epigenetics2011
5-Aza-2'-deoxycytidine stress response and apoptosis in prostate cancer.
Article in Clinical epigenetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.
- The clinicopathological significance and potential drug target of E-cadherin in NSCLC.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Pooled it
- The clinicopathological significance of CDH1 in gastric cancer: a meta-analysis and systematic review.Drug design, development and therapy · 2015Pooled it
- Role of DNA methylation transferase in urinary system diseases: From basic to clinical perspectives (Review).International journal of molecular medicine · 2025Review
- Tissue factor pathway inhibitor-2 (TFPI-2)-an underappreciated partaker in cancer and metastasis.Cancer metastasis reviews · 2024Review
- Aberrant promoter methylation contributes to LRIG1 silencing in basal/triple-negative breast cancer.British journal of cancer · 2022Article
- From Therapy Resistance to Targeted Therapies in Prostate Cancer.Frontiers in oncology · 2022Review
- The Differential Antitumor Activity of 5-Aza-2'-deoxycytidine in Prostate Cancer DU145, 22RV1, and LNCaP Cells.Journal of Cancer · 2021Article
- DNA methylation in development and disease: an overview for prostate researchers.American journal of clinical and experimental urology · 2018Review
- Low concentrations of 5-aza-2'-deoxycytidine induce breast cancer stem cell differentiation by triggering tumor suppressor gene expression.OncoTargets and therapy · 2016Article
- Genome-wide demethylation by 5-aza-2'-deoxycytidine alters the cell fate of stem/progenitor cells.Stem cell reviews and reports · 2015Article
- EHMT2 inhibitor BIX-01294 induces apoptosis through PMAIP1-USP9X-MCL1 axis in human bladder cancer cells.Cancer cell international · 2015Article
- Elucidation of caveolin 1 both as a tumor suppressor and metastasis promoter in light of epigenetic modulators.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- DNA methylation of E-cadherin is a priming mechanism for prostate development.Developmental biology · 2014Article
- Expression profiling of DNA methylation-mediated epigenetic gene-silencing factors in breast cancer.Clinical epigenetics · 2014Article
- Article
- 3-D DNA methylation phenotypes correlate with cytotoxicity levels in prostate and liver cancer cell models.BMC pharmacology & toxicology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While studying on epigenetic regulatory mechanisms (DNA methylation at C-5 of -CpG- cytosine and demethylation of methylated DNA) of certain genes (FAS, CLU, E-cadh, CD44, and Cav-1) associated with prostate cancer development and its better management, we noticed that the used in vivo dose of 5-aza-2'-deoxycytidine (5.0 to 10.0 nM, sufficient to inhibit DNA methyltransferase activity in vitro) helped in the transcription of various genes with known (steroid receptors, AR and ER; ER variants, CD44, CDH1, BRCA1, TGFβR1, MMP3, MMP9, and UPA) and unknown (DAZ and Y-chromosome specific) proteins and the respective cells remained healthy in culture. At a moderate dose (20 to 200 nM) of the inhibitor, cells remain growth arrested. Upon subsequent challenge with increased dose (0.5 to 5.0 μM) of the inhibitor, we observed that the cellular morphology was changing and led to death of the cells with progress of time. Analyses of DNA and anti-, pro-, and apoptotic factors of the affected cells revealed that the molecular events that went on are characteristics of programmed cell death (apoptosis).
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.