Evidence map›Paper›PMID 24754246›Full record

ArticleCancer science2014

Expression of CD24 is associated with HER2 expression and supports HER2-Akt signaling in HER2-positive breast cancer cells.

Mari Hosonaga, Yoshimi Arima, Eiji Sugihara, Norio Kohno, Hideyuki Saya

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Targeting CD24 as a novel immunotherapy for solid cancers.Cell communication and signaling : CCS · 2023
    Review
  8. Emerging Immune Checkpoint Molecules on Cancer Cells: CD24 and CD200.International journal of molecular sciences · 2023
    Review
  9. Article
  10. CD24: A Novel Target for Cancer Immunotherapy.Journal of personalized medicine · 2022
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. HER2 in stemness and epithelial-mesenchymal plasticity of breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Lapatinib resistance in HER2+ cancers: latest findings and new concepts on molecular mechanisms.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
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 3 institutions in 2 countries.

Mari HosonagaDivision of Gene Regulation, Institute for Advanced Medical Research, School of Medicine, Keio University, Tokyo, Japan; Department of Breast Oncology, Tokyo Medical University, Tokyo, Japan.
Yoshimi Arima
Eiji Sugihara
Norio Kohno
Hideyuki Saya
Keio University · JPTokyo Medical University · JPInstitute for Advanced Medical Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human epidermal growth factor receptor 2 (HER2)-positive breast cancer is treated with HER2-targeted agents, such as trastuzumab and lapatinib, that suppress signaling by phosphatidylinositol 3-kinase (PI3K)-Akt and MAPK pathways. However, resistance to HER2-targeted therapy remains a major clinical problem. Overexpression of CD24 has been detected in many cancers and is associated with a poor prognosis in women with breast cancer. HER2-positive breast tumors are predominantly positive for CD24, suggesting that the expression of the two molecules is related. To investigate the relation between HER2 and CD24, we overexpressed HER2 in breast cancer cells that were triple-negative for the estrogen receptor, progesterone receptor and HER2. We found that expression of CD24 was increased by stable overexpression of HER2. Flow cytometry thus revealed that the percentage of CD24-positive cells was markedly higher in the HER2-positive fraction than in the HER2-negative fraction. Knockdown of CD24 in breast cancer cells positive for endogenous HER2 downregulated HER2 expression, whereas knockdown of HER2 did not affect the expression of CD24. Knockdown of CD24 also suppressed the phosphorylation of Akt, which functions downstream of HER2 and PI3K to promote cell survival. Moreover, knockdown of CD24 increased the sensitivity of HER2-positive breast cancer cells to lapatinib treatment. Our results thus indicate that CD24 supports both the expression of HER2 and the consequent activation of PI3K-Akt signaling. Furthermore, CD24 may contribute to resistance to HER2-targeted therapy and, therefore, is itself a potential therapeutic target in HER2-positive breast cancer.

Indexed as

AnimalsBreast NeoplasmsCD24 AntigenCell Line, TumorErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLapatinibMiceMice, NudeMolecular Targeted TherapyNeoplastic Stem CellsPhosphatidylinositol 3-KinasesPhosphorylationCD24 AntigenCD24 protein, humanERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesLapatinibPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktQuinazolinesAktbreast cancerCD24human epidermal growth factor receptor 2PI3K

Identifiers

PMID24754246
PMCPMC4317915
OpenAlexW1994130324

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.