Evidence map›Paper›PMID 20331626›Full record

ArticleCancer science2010

Inhibition of ErbB2 by Herceptin reduces survivin expression via the ErbB2-beta-catenin/TCF4-survivin pathway in ErbB2-overexpressed breast cancer cells.

Hongxia Zhu, Guo Zhang, Yan Wang, Ninghong Xu, Shun He, Wei Zhang, Meigui Chen, Mei Liu, Lanping Quan, Jingfeng Bai and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-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

14 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Pulmonary epithelial barrier function: some new players and mechanisms.American journal of physiology. Lung cellular and molecular physiology · 2015
    Review
  7. HER2 activation results in β-catenin-dependent changes in pulmonary epithelial permeability.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  8. Article
  9. Article
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  11. Article
  12. Article
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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

11 authors at 4 institutions in 2 countries.

Hongxia ZhuLaboratory of Cell and Molecular Biology, State Key Laboratory of Molecular Oncology, Beijing, China.
Guo Zhang
Yan Wang
Ninghong Xu
Shun He
Wei Zhang
Meigui Chen
Mei Liu
Lanping Quan
Jingfeng Bai
Ningzhi Xu
Molecular Oncology (United States) · USState Key Laboratory of Molecular OncologyLoudi Central Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overexpression of ErbB2 is associated with poor prognosis in breast cancer. Targeting of ErbB2 is a very common therapeutic strategy in ErbB2-overexpressed breast cancer. Herceptin is the first approved and most widely used agent for ErbB2-targeting therapy in breast cancer. Even though the clinical application has been performed for more than 10 years, the exact mechanism underlying how Herceptin exhibits its effects has not been fully elucidated. In this study, we found that Herceptin could inhibit the expression of survivin in ErbB2-overexpressed cell lines. Overexpression of survivin could abrogate the inhibition of cell growth induced by Herceptin. Herceptin could reduce survivin expression at the transcriptional level. The beta-catenin/T-cell factor (TCF) pathway played a very crucial role in this cascade. We found that Herceptin could reduce tyrosine phosphorylation levels of ErbB2 and beta-catenin. Herceptin treatment induced degradation of beta-catenin protein, resulting in reduced binding affinity of beta-catenin/TCF4 to the promoter region of survivin. When we cross-mutated the TCF4 binding sites in the promoter region of survivin, the reduction of survivin promoter activity almost diminished. Taken together, we showed that Herceptin could inhibit survivin expression through the ErbB2-beta-catenin/TCF4-survivin pathway in ErbB2-overexpressed breast cancer cells. This indicates that there may be a new cascade axis from ErbB2 to survivin.

Indexed as

Antibodies, MonoclonalAntibodies, Monoclonal, HumanizedBasic Helix-Loop-Helix Leucine Zipper Transcription Factorsbeta CateninBreast NeoplasmsCell Line, TumorErb-b2 Receptor Tyrosine KinasesFemaleHumansInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSurvivinTranscription Factor 4Transcription FactorsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedBasic Helix-Loop-Helix Leucine Zipper Transcription Factorsbeta CateninBIRC5 protein, humanERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSurvivinTCF4 protein, humanTranscription Factor 4Transcription FactorsTrastuzumab

Identifiers

PMID20331626
PMCPMC11158864
OpenAlexW2081467880

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.