Evidence map›Paper›PMID 22266859›Full record

ArticleOncogene2012

Androgen-regulated miR-32 targets BTG2 and is overexpressed in castration-resistant prostate cancer.

S E Jalava, A Urbanucci, L Latonen, K K Waltering, B Sahu, O A Jänne, J Seppälä, H Lähdesmäki, T L J Tammela, T Visakorpi

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 2 pooled it
10.3field-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

117 citing papers in PubMed, 2 syntheses or guidelines pooled it, 224 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. MicroRNA-409-3p/BTG2 signaling axis improves impaired angiogenesis and wound healing in obese mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  11. Review
  12. Article
  13. Review
  14. microRNA-205 in prostate cancer: Overview to clinical translation.Biochimica et biophysica acta. Reviews on cancer · 2022
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review

57 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

10 authors at 4 institutions in 1 country.

S E JalavaInstitute of Biomedical Technology, Tampere University, Tampere, Finland.
A Urbanucci
L Latonen
K K Waltering
B Sahu
O A Jänne
J Seppälä
H Lähdesmäki
T L J Tammela
T Visakorpi
Tampere University · FITampere University · FIUniversity of Helsinki · FIAalto University · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The androgen receptor (AR) signaling pathway is involved in the emergence of castration-resistant prostate cancer (CRPC). Here, we identified several androgen-regulated microRNAs (miRNAs) that may contribute to the development of CRPC. Seven miRNAs, miR-21, miR-32, miR-99a, miR-99b, miR-148a, miR-221 and miR-590-5p, were found to be differentially expressed in CRPC compared with benign prostate hyperplasia (BPH) according to microarray analyses. Significant growth advantage for LNCaP cells transfected with pre-miR-32 and pre-miR-148a was found. miR-32 was demonstrated to reduce apoptosis, whereas miR-148a enhanced proliferation. Androgen regulation of miR-32 and miR-148a was confirmed by androgen stimulation of the LNCaP cells followed by expression analyses. The AR-binding sites in proximity of these miRNAs were demonstrated with chromatin immunoprecipitation (ChIP). To identify target genes for the miRNAs, mRNA microarray analyses were performed with LNCaP cells transfected with pre-miR-32 and pre-miR-148a. Expression of BTG2 and PIK3IP1 was reduced in the cells transfected with pre-miR-32 and pre-miR-148a, respectively. Also, the protein expression was reduced according to western blot analysis. BTG2 and PIK3IP1 were confirmed to be targets by 3'UTR-luciferase assays. Finally, immunostainings showed a statistically significant (P<0.0001) reduction of BTG2 protein in CRPCs compared with untreated prostate cancer (PC). The lack of BTG2 staining was also associated (P<0.01) with a short progression-free time in patients who underwent prostatectomy. In conclusion, androgen-regulated miR-32 is overexpressed in CRPC, leading to reduced expression of BTG2. Thus, miR-32 is a potential marker for aggressive disease and is a putative drug target in PC.

Indexed as

Gene Expression Regulation, NeoplasticAndrogensBinding SitesCase-Control StudiesCell Line, TumorCell ProliferationHumansImmediate-Early ProteinsIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsMicroRNAsNeoplasms, Hormone-DependentOligonucleotide Array Sequence AnalysisPrognosisProstatic NeoplasmsAndrogensBTG2 protein, humanImmediate-Early ProteinsIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicroRNAsMIRN148 microRNA, humanMIRN32 microRNA, humanPIK3IP1 protein, humanReceptors, AndrogenTumor Suppressor Proteins

Identifiers

PMID22266859
OpenAlexW1981298542

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.