Evidence map›Paper›PMID 19252524›Full record

ArticleOncogene2009

miR-449a targets HDAC-1 and induces growth arrest in prostate cancer.

E J Noonan, R F Place, D Pookot, S Basak, J M Whitson, H Hirata, C Giardina, R Dahiya

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
188citing papers in PubMed, 3 pooled it
17.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

188 citing papers in PubMed, 3 syntheses or guidelines pooled it, 389 citations in OpenAlex.

  1. Pooled it
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  11. HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
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  18. Navigating the genomic instability mine field of osteosarcoma to better understand implications of non-coding RNAs.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2022
    Article
  19. Article
  20. Article

128 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

E J NoonanDepartment of Urology, Veterans Affairs Medical Center and University of California, San Francisco, CA 94121, USA. emily.noonan@gmail.com
R F Place
D Pookot
S Basak
J M Whitson
H Hirata
C Giardina
R Dahiya
University of California, San Francisco · USSan Francisco VA Medical Center · USUniversity of Connecticut · US

Funding

CYP1A1 and CYP1B1 genes in race-related Prostate CancerR01CA101844 · NCI · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI DAHIYA, RAJVIR · 2003 to 2007
$1.4M
UROLOGICAL RESEARCH TRAINING PROGRAMT32DK007790 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DAHIYA, RAJVIR · 2000 to 2011
$812k
NCI NIH HHS R01CA101844NCI NIH HHS R01CA111470SNIDDK NIH HHS T32DK007790
6 · The paper itself

Abstract

Histone deacetylases (HDACs) are frequently overexpressed in broad range of cancer types, where they alter cellular epigenetic programming to promote cell proliferation and survival. However, the mechanism by which HDACs become overexpressed in human cancers remains somewhat of a mystery. In this study, we investigated the expression and functional significance of miR-449a in prostate cancer cells. Using real-time PCR, we found that miR-449a is downregulated in prostate cancer tissues relative to patient-matched control tissue. Introduction of miR-449a into PC-3 prostate cancer cells resulted in cell-cycle arrest, apoptosis and a senescent-like phenotype. In silico analysis of 3'-UTR regions identified a number of genes involved in cell-cycle regulation as putative targets of miR-449a. Using a luciferase 3'-UTR reporter system, we established that HDAC-1 (histone deacetylase 1), a gene that is frequently overexpressed in many types of cancer, is a direct target of miR-449a. Further, our data indicate that miR-449a regulates cell growth and viability in part by repressing the expression of HDAC-1 in prostate cancer cells. Our findings provide new insight into the function of miRNA in regulating HDAC expression in normal versus cancerous tissue.

Indexed as

Histone Deacetylase InhibitorsCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p27Gene Expression Regulation, EnzymologicHistone Deacetylase 1HumansIntracellular Signaling Peptides and ProteinsMaleMicroRNAsPhenotypeProstatic NeoplasmsRNA, Small InterferingCDKN1B protein, humanCyclin-Dependent Kinase Inhibitor p27HDAC1 protein, humanHistone Deacetylase 1Histone Deacetylase InhibitorsIntracellular Signaling Peptides and ProteinsMicroRNAsRNA, Small Interfering

Identifiers

PMID19252524
OpenAlexW2001502548

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.