Evidence map›Paper›PMID 34341513›Full record

ArticleOncogene2021

CRYβB2 enhances tumorigenesis through upregulation of nucleolin in triple negative breast cancer.

Yu Yan, Athira Narayan, Soonweng Cho, Zhiqiang Cheng, Jun O Liu, Heng Zhu, Guannan Wang, Bryan Wharram, Ala Lisok, Mary Brummet and 13 more

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

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

10 citing papers in PubMed, 13 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

23 authors at 5 institutions in 2 countries.

Yu YanDepartment of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID http://orcid.org/0000-0003-2309-9464
Athira NarayanDepartment of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Soonweng ChoDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Zhiqiang ChengDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Jun O LiuDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID http://orcid.org/0000-0003-3842-9841
Heng ZhuDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID http://orcid.org/0000-0002-8426-2889
Guannan WangDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Bryan WharramDepartment of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID http://orcid.org/0000-0002-5132-4000
Ala LisokDepartment of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Mary BrummetDepartment of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Harumi SaekiDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID http://orcid.org/0000-0001-8569-1872
Tao HuangDepartment of Breast and Thyroid Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Kathleen GabrielsonDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Edward GabrielsonDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Leslie CopeDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Yasmine M KanaanDepartment of Microbiology, College of Medicine, Howard University, Washington, DC, USA.
Ali AfsariDepartment of Pathology, College of Medicine, Howard University, Washington, DC, USA.
Tammey NaabDepartment of Pathology, College of Medicine, Howard University, Washington, DC, USA.
Harris G YfantisPathology and Laboratory Medicine, Baltimore Veterans Affairs Medical Center, Baltimore, MD, USA.
Stefan AmbsMolecular Epidemiology Section, Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0001-7651-9309
Martin G PomperDepartment of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Saraswati SukumarDepartment of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. saras@jhmi.edu.ORCID http://orcid.org/0000-0002-5656-6703
Vanessa F MerinoDepartment of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA. vmerino1@jhmi.edu.ORCID http://orcid.org/0000-0003-2251-2309
Johns Hopkins University · USHoward University · USUnion Hospital · CNNational Institutes of Health · USVeterans Health Administration · US

Funding

Novel Markers for Disease Outcome in Breast CancerZIABC010887 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI AMBS, STEFAN · 2009 to 2025
$11.5M
Intramural NIH HHS ZIA BC010887
6 · The paper itself

Abstract

Expression of β-crystallin B2 (CRYβB2) is elevated in African American (AA) breast tumors. The underlying mechanisms of CRYβB2-induced malignancy and the association of CRYβB2 protein expression with survival have not yet been described. Here, we report that the expression of CRYβB2 in breast cancer cells increases stemness, growth, and metastasis. Transcriptomics data revealed that CRYβB2 upregulates genes that are functionally associated with unfolded protein response, oxidative phosphorylation, and DNA repair, while down-regulating genes related to apoptosis. CRYβB2 in tumors promotes de-differentiation, an increase in mesenchymal markers and cancer-associated fibroblasts, and enlargement of nucleoli. Proteome microarrays identified a direct interaction between CRYβB2 and the nucleolar protein, nucleolin. CRYβB2 induces nucleolin, leading to the activation of AKT and EGFR signaling. CRISPR studies revealed a dependency on nucleolin for the pro-tumorigenic effects of CRYβB2. Triple-negative breast cancer (TNBC) xenografts with upregulated CRYβB2 are distinctively sensitive to the nucleolin aptamer, AS-1411. Lastly, in AA patients, higher levels of nucleolar CRYβB2 in primary TNBC correlates with decreased survival. In summary, CRYβB2 is upregulated in breast tumors of AA patients and induces oncogenic alterations consistent with an aggressive cancer phenotype. CRYβB2 increases sensitivity to nucleolin inhibitors and may promote breast cancer disparity.

Indexed as

Up-RegulationAnimalsAptamers, Nucleotidebeta-Crystallin B ChainCell NucleolusCell ProliferationFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMiceNeoplasm InvasivenessNeoplasm TransplantationNeoplastic Stem CellsNucleolinOligodeoxyribonucleotidesAGRO 100Aptamers, Nucleotidebeta-crystallin B2beta-Crystallin B ChainNucleolinOligodeoxyribonucleotidesPhosphoproteinsRNA-Binding Proteins

Identifiers

PMID34341513
PMCPMC10064491
OpenAlexW3192369490

What OpenQuestion holds

Textmetadata
LicenceTDM
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.