Evidence map›Paper›PMID 21532615›Full record

ArticleOncogene2011

Control of tumor and microenvironment cross-talk by miR-15a and miR-16 in prostate cancer.

M Musumeci, V Coppola, A Addario, M Patrizii, M Maugeri-Saccà, L Memeo, C Colarossi, F Francescangeli, M Biffoni, D Collura and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed, 1 pooled it
9.3field-weighted citation impact, top 2% 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

131 citing papers in PubMed, 1 synthesis or guideline pooled it, 240 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Review
  6. Article
  7. A novel intronic circular RNA circFGFR1Journal of translational medicine · 2023
    Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. miRNA: A Promising Therapeutic Target in Cancer.International journal of molecular sciences · 2022
    Review
  14. MicroRNAs and Heat Shock Proteins in Breast Cancer Biology.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  15. Analysis of the p53/microRNA Network in Cancer.Advances in experimental medicine and biology · 2022
    Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Patient-Derived Organoids as a Model for Cancer Drug Discovery.International journal of molecular sciences · 2021
    Review

71 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

17 authors at 2 institutions in 1 country.

M MusumeciDepartment of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
V Coppola
A Addario
M Patrizii
M Maugeri-Saccà
L Memeo
C Colarossi
F Francescangeli
M Biffoni
D Collura
A Giacobbe
L D'Urso
M Falchi
M A Venneri
G Muto
R De Maria
D Bonci
Istituto Superiore di Sanità · ITOspedale San Giovanni Bosco · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interaction between cancer cells and microenvironment has a critical role in tumor development and progression. Although microRNAs regulate all the major biological mechanisms, their influence on tumor microenvironment is largely unexplored. Here, we investigate the role of microRNAs in the tumor-supportive capacity of stromal cells. We demonstrated that miR-15 and miR-16 are downregulated in fibroblasts surrounding the prostate tumors of the majority of 23 patients analyzed. Such downregulation of miR-15 and miR-16 in cancer-associated fibroblasts (CAFs) promoted tumor growth and progression through the reduced post-transcriptional repression of Fgf-2 and its receptor Fgfr1, which act on both stromal and tumor cells to enhance cancer cell survival, proliferation and migration. Moreover, reconstitution of miR-15 and miR-16 impaired considerably the tumor-supportive capability of stromal cells in vitro and in vivo. Our data suggest a molecular circuitry in which miR-15 and miR-16 and their correlated targets cooperate to promote tumor expansion and invasiveness through the concurrent activity on stromal and cancer cells, thus providing further support to the development of therapies aimed at reconstituting miR-15 and miR-16 in advanced prostate cancer.

Indexed as

AgedAged, 80 and overAnimalsBlotting, WesternCell Line, TumorDown-RegulationFibroblast Growth Factor 2FibroblastsGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred NODMice, SCIDMicroRNAsMiddle AgedFibroblast Growth Factor 2MicroRNAsMIRN15 microRNA, humanMIRN16 microRNA, humanProto-Oncogene Proteins c-aktReceptor, Fibroblast Growth Factor, Type 1

Identifiers

PMID21532615
OpenAlexW1963966397

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.