Evidence map›Paper›PMID 30719702›Full record

ArticleInternational journal of cancer2019

β1 Integrin is essential for fascin-mediated breast cancer stem cell function and disease progression.

Rayanah Barnawi, Samiyah Al-Khaldi, Dilek Colak, Asma Tulbah, Taher Al-Tweigeri, Mohannad Fallatah, Dorota Monies, Hazem Ghebeh, Monther Al-Alwan

Open access · hybridAbstract read
In one paragraph

Article in International journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 56 citations in OpenAlex.

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  13. Integrins in cancer stem cells.Frontiers in cell and developmental biology · 2024
    Review
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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

9 authors at 3 institutions in 1 country.

Rayanah BarnawiStem Cell and Tissue Re-Engineering Program, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.
Samiyah Al-KhaldiNational Center for Stem Cells, Life Science and Environment Research Institute, King Abdulaziz City for Sciences and Technology, Riyadh, Saudi Arabia.
Dilek ColakDepartment of Biostatistics, Epidemiology and Scientific Computing, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.
Asma TulbahDepartment of Pathology and Laboratory Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.
Taher Al-TweigeriDepartment of Oncology, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.
Mohannad FallatahNational Center for Stem Cells, Life Science and Environment Research Institute, King Abdulaziz City for Sciences and Technology, Riyadh, Saudi Arabia.
Dorota MoniesDepartment of Genetics, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.
Hazem GhebehStem Cell and Tissue Re-Engineering Program, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.ORCID 0000-0002-3297-3996
Monther Al-AlwanStem Cell and Tissue Re-Engineering Program, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.ORCID 0000-0003-2150-5297
King Faisal Specialist Hospital & Research Centre · SAAlfaisal University · SAKing Abdulaziz City for Science and Technology · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer remains the second cause of tumor-related mortality in women worldwide mainly due to chemoresistance and metastasis. The chemoresistance and metastasis are attributed to a rare subpopulation with enriched stem-like characteristics, thus called Cancer Stem Cells (CSCs). We have previously reported aberrant expression of the actin-bundling protein (fascin) in breast cancer cells, which enhances their chemoresistance, metastasis and enriches CSC population. The intracellular mechanisms that link fascin with its downstream effectors are not fully elucidated. Here, loss and gain of function approaches in two different breast cancer models were used to understand how fascin promotes disease progression. Importantly, findings were aligned with expression data from actual breast cancer patients. Expression profiling of a large breast cancer dataset (TCGA, 530 patients) showed statistically significant correlation between fascin expression and a key adherence molecule, β1 integrin (ITGB1). In vitro manipulation of fascin expression in breast cancer cells exhibited its direct effect on ITGB1 expression. Fascin-mediated regulation of ITGB1 was critical for several breast cancer cell functions including adhesion to different extracellular matrix, self-renewability and chemoresistance. Importantly, there was a significant relationship between fascin and ITGB1 co-expression and short disease-free as well as overall survival in chemo-treated breast cancer patients. This novel role of fascin effect on ITGB1 expression and its outcome on cell self-renewability and chemoresistance strongly encourages for dual targeting of fascin-ITGB1 axis as a therapeutic approach to halt breast cancer progression and eradicate it from the root.

Indexed as

Breast NeoplasmsCarrier ProteinsCell AdhesionCell Line, TumorDisease ProgressionFemaleGene ExpressionHumansImmunohistochemistryIntegrin beta1Microfilament ProteinsNeoplastic Stem CellsSurvival AnalysisUp-RegulationCarrier ProteinsfascinIntegrin beta1Microfilament Proteinsbreast cancercancer stem cellfascinintegrinsITGB1β1 integrin

Identifiers

PMID30719702
PMCPMC6593770
OpenAlexW2912237116

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.