Evidence map›Paper›PMID 27542246›Full record

ArticleOncotarget2016

Nucleolin-binding by ErbB2 enhances tumorigenicity of ErbB2-positive breast cancer.

Eya Wolfson, Maria Goldenberg, Shira Solomon, Amit Frishberg, Ronit Pinkas-Kramarski

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Cancer Stem Cells and Nucleolin as Drivers of Carcinogenesis.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  10. International journal of nanomedicine · 2021
    Article
  11. Article
  12. Frontiers in cell and developmental biology · 2021
    Article
  13. Article
  14. The nucleolus, an ally, and an enemy of cancer cells.Histochemistry and cell biology · 2018
    Review
  15. DruggableCancers · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. 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

5 authors at 1 institution in 1 country.

Eya WolfsonDepartment of Neurobiology, Tel-Aviv University, Ramat-Aviv, 69978, Israel.
Maria GoldenbergDepartment of Neurobiology, Tel-Aviv University, Ramat-Aviv, 69978, Israel.
Shira SolomonDepartment of Neurobiology, Tel-Aviv University, Ramat-Aviv, 69978, Israel.
Amit FrishbergDepartment of Cell Research and Immunology, Tel-Aviv University, Ramat-Aviv, 69978, Israel.
Ronit Pinkas-KramarskiDepartment of Neurobiology, Tel-Aviv University, Ramat-Aviv, 69978, Israel.
Tel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ErbB2 is an important member of the ErbB family, which activates growth and proliferation signaling pathways. ErbB2 is often overexpressed in various malignancies, especially in breast cancer, and is a common target for anti-cancer drugs. Breast cancer is currently one of the leading mortality causes in women, and acquired resistance to ErbB2-targeted therapies is a major obstacle in its treatment. Thus, understanding ErbB2-mediated signaling is crucial for further development of anti-cancer therapeutics and disease treatment. Previously, we have reported that the ErbB receptors interact with the major nucleolar protein nucleolin. In addition to its function in the nucleoli of cells, nucleolin participates in various cellular processes at the cytoplasm and cell-surface. Deregulated nucleolin is frequently overexpressed on the membrane of cancer cells. Here, we show that nucleolin increases colony formation and anchorage-independent growth of ErbB2-overexpressing cells. Importantly, this enhanced tumorigenicity also occurs in human ErbB2-positive breast cancer patients; namely, nucleolin overexpression in these patients is associated with reduced patient survival rates and increased disease-risk. ErbB2-nucleolin complexes are formed endogenously in both normal and cancer cells, and their effect on tumorigenicity is mediated through activation of ErbB2 signaling. Accordingly, nucleolin inhibition reduces cell viability and ErbB2 activation in ErbB2-positive cancer cells.

Indexed as

Antineoplastic AgentsBreast NeoplasmsCarcinogenesisCell AdhesionCell Growth ProcessesCell Line, TumorDrug Resistance, NeoplasmErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, NeoplasticHEK293 CellsHumansMolecular Targeted TherapyNucleolinPhosphoproteinsProtein BindingAntineoplastic AgentsERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesNucleolinPhosphoproteinsRNA-Binding ProteinsRNA, Small Interferingbreast cancerErbB/HER familynucleolinTCGAtyrosine kinase

Identifiers

PMID27542246
PMCPMC5323158
OpenAlexW2508346351

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.