Evidence map›Paper›PMID 31496817›Full record

ArticleCancer management and research2019

OSM-induced CD44 contributes to breast cancer metastatic potential through cell detachment but not epithelial-mesenchymal transition.

Hunter Covert, Liliana F Mellor, Cody L Wolf, Nicole Ankenbrandt, Jacqueline M Emathinger, Ken Tawara, Julie Thom Oxford, Cheryl L Jorcyk

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

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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 1 institution in 2 countries.

Hunter CovertBoise State University, Biomolecular Sciences Program, Boise, ID 83725, USA.
Liliana F MellorBoise State University, Department of Biological Sciences, Boise, ID 83725, USA.
Cody L WolfBoise State University, Biomolecular Sciences Program, Boise, ID 83725, USA.
Nicole AnkenbrandtBoise State University, Biomolecular Sciences Program, Boise, ID 83725, USA.
Jacqueline M EmathingerBoise State University, Department of Biological Sciences, Boise, ID 83725, USA.
Ken TawaraBoise State University, Biomolecular Sciences Program, Boise, ID 83725, USA.
Julie Thom OxfordBoise State University, Biomolecular Sciences Program, Boise, ID 83725, USA.
Cheryl L JorcykBoise State University, Biomolecular Sciences Program, Boise, ID 83725, USA.
Boise State University · US

Funding

Women's health: interplay of maternal diet and key demographics on neurological health in the rural frontier and remote WestP20GM103408 · NIGMS · UNIVERSITY OF IDAHO · PI Scott A Minnich · 2012 to 2026
$59.8M
UNDERGRADUATE COLLEGE OUTREACH PROGRAMP20RR016454 · NCRR · UNIVERSITY OF IDAHO · PI SIMPKIN, JANICE L · 2001 to 2011
$35.3M
VPS35 D620N inhibits autophagy through disrupted hyaluronic acid-CD44 signalingP20GM109095 · NIGMS · BOISE STATE UNIVERSITY · PI OCHOA-REPARAZ, JAVIER · 2014 to 2023
$22.7M
Oncostatin M-induced VEGF in human breast cancer is HIF1a-mediatedR15CA137510 · NCI · BOISE STATE UNIVERSITY · PI JORCYK, CHERYL LYNN · 2009 to 2009
$212k
NCI NIH HHS R15 CA137510NCRR NIH HHS P20 RR016454NIGMS NIH HHS P20 GM103408NIGMS NIH HHS P20 GM109095
6 · The paper itself

Abstract

backgroundHormone receptor status in human breast cancer cells is a strong indicator of the aggressiveness of a tumor. Triple negative breast cancers (TNBC) are aggressive, difficult to treat, and contribute to high incidences of metastasis by possessing characteristics such as increased tumor cell migration and a large presence of the transmembrane protein, cluster of differentiation 44 (CD44) on the cell membrane. Estrogen receptor-positive (ER+) cells are less aggressive and do not migrate until undergoing an epithelial-mesenchymal transition (EMT).

methodsThe relationship between EMT and CD44 during metastatic events is assessed by observing changes in EMT markers, tumor cell detachment, and migration following cytokine treatment on both parental and CD44 knockdown human breast tumor cells.

resultsER+ T47D and MCF-7 human breast cancer cells treated with OSM demonstrate increased CD44 expression and CD44 cleavage. Conversely, ER- MDA-MB-231 human breast cancer cells do not show a change in CD44 expression nor undergo EMT in the presence of OSM. In ER+ cells, knockdown expression of CD44 by shRNA did not prevent EMT but did change metastatic processes such as cellular detachment and migration. OSM-induced migration was decreased in both ER+ and ER- cells with shCD44 cells compared to control cells, while the promotion of tumor cell detachment by OSM was decreased in ER+ MCF7-shCD44 cells, as compared to control cells. Interestingly, OSM-induced detachment in ER- MDA-MB-231-shCD44 cells that normally don't detach at significant rates.

conclusionOSM promotes both EMT and tumor cell detachment in ER+ breast cancer cells. Yet, CD44 knockdown did not affect OSM-induced EMT in these cells, while independently decreasing OSM-induced cell detachment. These results suggest that regulation of CD44 by OSM is important for at least part of the metastatic cascade in ER+ breast cancer.

Indexed as

breast tumor metastasiscluster of differentiation 44epithelial to mesenchymal transitionOncostatin M

Identifiers

PMID31496817
PMCPMC6700398
OpenAlexW2967955868

What Socratic holds

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LicenceCC BY-NC
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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 Socratic graph.