Evidence map›Paper›PMID 23584474›Full record

ArticleOncogene2014

Oncostatin-M promotes phenotypic changes associated with mesenchymal and stem cell-like differentiation in breast cancer.

N R West, J I Murray, P H Watson

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 105 citations in OpenAlex.

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  15. gp130 Cytokines Activate Novel Signaling Pathways and Alter Bone Dissemination in ER+ Breast Cancer Cells.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
  16. A novel immune prognostic model of non-M3 acute myeloid leukemia.American journal of translational research · 2022
    Article
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6 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

3 authors at 1 institution in 1 country.

N R West1] Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia, Canada [2] Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia, Canada.
J I MurrayDeeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia, Canada.
P H Watson1] Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia, Canada [2] Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia, Canada [3] Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
BC Cancer Agency · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem cell (CSC) biology and the epithelial-to-mesenchymal transition (EMT) are thought to be mechanistically linked and may be key components of cancer development and progression. However, stimuli that induce EMT and CSC-like features ('stemness') are poorly defined. We and others have shown that the inflammatory cytokine oncostatin-M (OSM) mediates phenotypic changes in breast cancer that are consistent with EMT and dedifferentiation, including enhanced migration and loss of hormone receptors. In this study, we have expanded on these prior observations to determine whether OSM is a cell-extrinsic driver of EMT and/or stemness. OSM stimulation of the luminal breast cancer cell lines MCF7 and T47D induced EMT features including loss of membranous E-cadherin and induction of snail and slug expression. OSM treatment markedly enhanced the formation of mammospheres (up to 20-fold, P<0.001), which displayed high expression of the pluripotency factor SOX2. The proportion of cells with a CD44(high)CD24(-/low) phenotype was similarly increased by OSM (P<0.001). OSM-induced mammosphere formation and CD44(high)CD24(-/low) induction was dependent on PI3K signalling. In silico analysis of human breast tumours (from a publicly available data set, n=322) confirmed that co-expression of a PI3K transcriptional signature, but not MAPK or STAT3 signatures, was necessary to detect an association between OSMR and poor prognosis. Assessment of a second in silico data set (n=241 breast tumours) confirmed a significant relationship between OSMR, markers of EMT and CSCs, and chemotherapy resistance. Direct analysis of mRNA expression by RT-PCR in a third cohort (n=72 breast tumours) demonstrated that high expression of OSM is associated positively with indicators of EMT (SNAI1, P<0.001) and stemness (SOX2, P<0.05). Our data suggest for the first time that OSM may promote a clinically relevant EMT/CSC-like phenotype in human breast cancer via a PI3K-dependent mechanism.

Indexed as

Cell DifferentiationPhenotypeBreast NeoplasmsCD24 AntigenEpithelial-Mesenchymal TransitionHumansHyaluronan ReceptorsMCF-7 CellsMesodermNeoplastic Stem CellsOncostatin MPhosphatidylinositol 3-KinasesSignal TransductionCD24 AntigenHyaluronan ReceptorsOncostatin MPhosphatidylinositol 3-Kinases

Identifiers

PMID23584474
OpenAlexW2029520352

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.