Evidence map›Paper›PMID 24370273›Full record

ArticleBMC cancer2013

Molecular signaling pathways mediating osteoclastogenesis induced by prostate cancer cells.

Shahrzad Rafiei, Svetlana V Komarova

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Prostate Cancer and Bone Metastases: The Underlying Mechanisms.International journal of molecular sciences · 2019
    Review
  7. Article
  8. PRDX4 and Its Roles in Various Cancers.Technology in cancer research & treatment · 2019
    Review
  9. [Molecular imaging and biology · 2017
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Osteoblast menin regulates bone mass in vivo.The Journal of biological chemistry · 2015
    Article
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

2 authors at 1 institution in 1 country.

Shahrzad Rafiei
Svetlana V KomarovaDepartment of Anatomy and Cell Biology, Faculty of Medicine, 3640 University Street, Montreal, Quebec H3A 2B2, Canada. svetlana.komarova@mcgill.ca.
Université de Montréal · CA

Funding

Canadian Institutes of Health Research MOP-77643
6 · The paper itself

Abstract

backgroundAdvanced prostate cancer commonly metastasizes to bone leading to osteoblastic and osteolytic lesions. Although an osteolytic component governed by activation of bone resorbing osteoclasts is prominent in prostate cancer metastasis, the molecular mechanisms of prostate cancer-induced osteoclastogenesis are not well-understood.

methodsWe studied the effect of soluble mediators released from human prostate carcinoma cells on osteoclast formation from mouse bone marrow and RAW 264.7 monocytes.

resultsSoluble factors released from human prostate carcinoma cells significantly increased viability of naïve bone marrow monocytes, as well as osteoclastogenesis from precursors primed with receptor activator of nuclear factor κ-B ligand (RANKL). The prostate cancer-induced osteoclastogenesis was not mediated by RANKL as it was not inhibited by osteoprotegerin (OPG). However inhibition of TGFβ receptor I (TβRI), or macrophage-colony stimulating factor (MCSF) resulted in attenuation of prostate cancer-induced osteoclastogenesis. We characterized the signaling pathways induced in osteoclast precursors by soluble mediators released from human prostate carcinoma cells. Prostate cancer factors increased basal calcium levels and calcium fluctuations, induced nuclear localization of nuclear factor of activated t-cells (NFAT)c1, and activated prolonged phosphorylation of ERK1/2 in RANKL-primed osteoclast precursors. Inhibition of calcium signaling, NFATc1 activation, and ERK1/2 phosphorylation significantly reduced the ability of prostate cancer mediators to stimulate osteoclastogenesis.

conclusionsThis study reveals the molecular mechanisms underlying the direct osteoclastogenic effect of prostate cancer derived factors, which may be beneficial in developing novel osteoclast-targeting therapeutic approaches.

Indexed as

Calcium SignalingMAP Kinase Signaling SystemAnimalsBone NeoplasmsCell CommunicationCell DifferentiationCell Line, TumorCell SurvivalCulture Media, ConditionedHumansMaleMiceMice, Inbred BALB CNFATC Transcription FactorsOsteoclastsProstatic NeoplasmsCulture Media, ConditionedNFATC1 protein, humanNFATC Transcription Factors

Identifiers

PMID24370273
PMCPMC3881018
OpenAlexW2081141707

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.