Evidence map›Paper›PMID 24707474›Full record

ArticleBioMed research international2014

Trichostatin A suppresses EGFR expression through induction of microRNA-7 in an HDAC-independent manner in lapatinib-treated cells.

Chih-Yen Tu, Chia-Hung Chen, Te-Chun Hsia, Min-Hsiang Hsu, Ya-Ling Wei, Meng-Chieh Yu, Wen-Shu Chen, Ke-Wei Hsu, Ming-Hsin Yeh, Liang-Chih Liu and 2 more

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

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  3. Review
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  7. Article
  8. Article
  9. Review
  10. Clinical Potential of microRNA-7 in Cancer.Journal of clinical medicine · 2015
    Review
  11. 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

12 authors at 5 institutions in 1 country.

Chih-Yen TuDivision of Pulmonary and Critical Care Medicine, China Medical University and Hospital, Taichung 404, Taiwan ; Department of Internal Medicine, China Medical University and Hospital, Taichung 404, Taiwan ; School of Medicine, China Medical University, Taichung 404, Taiwan ; Department of Life Science, National Chung-Hsing University, Taichung 402, Taiwan.ORCID 0000-0002-8126-6171
Chia-Hung ChenDivision of Pulmonary and Critical Care Medicine, China Medical University and Hospital, Taichung 404, Taiwan ; Department of Internal Medicine, China Medical University and Hospital, Taichung 404, Taiwan ; Department of Respiratory Therapy, China Medical University, Taichung 404, Taiwan ; Graduate Institute of Clinical Medical Science, China Medical University, Taichung 404, Taiwan.
Te-Chun HsiaDepartment of Internal Medicine, China Medical University and Hospital, Taichung 404, Taiwan ; Department of Respiratory Therapy, China Medical University, Taichung 404, Taiwan.
Min-Hsiang HsuGraduate Institute of Cancer Biology, China Medical University, Taichung 404, Taiwan.
Ya-Ling WeiCenter for Molecular Medicine, China Medical University and Hospital, Taichung 404, Taiwan.
Meng-Chieh YuDepartment of Internal Medicine, China Medical University and Hospital, Taichung 404, Taiwan ; Graduate Institute of Cancer Biology, China Medical University, Taichung 404, Taiwan.
Wen-Shu ChenCenter for Molecular Medicine, China Medical University and Hospital, Taichung 404, Taiwan ; Department of Pharmacology, College of Medicine, National Taiwan University, Taipei 106, Taiwan.
Ke-Wei HsuDepartment of Biological Science and Technology, China Medical University, Taichung 404, Taiwan.
Ming-Hsin YehSection of Breast Surgery, China Medical University and Hospital, Taichung 404, Taiwan.
Liang-Chih LiuSchool of Medicine, China Medical University, Taichung 404, Taiwan ; Department of Surgery, China Medical University and Hospital, Taichung 404, Taiwan.
Yun-Ju ChenDepartment of Medical Research, E-Da Hospital, Kaohsiung 824, Taiwan ; Department of Biological Science & Technology, I-Shou University, Kaohsiung 824, Taiwan.
Wei-Chien HuangGraduate Institute of Cancer Biology, China Medical University, Taichung 404, Taiwan ; Center for Molecular Medicine, China Medical University and Hospital, Taichung 404, Taiwan ; The Ph.D. Program for Cancer Biology and Drug Discovery, China Medical University, Taichung 404, Taiwan ; Department of Biotechnology, Asia University, Taichung 413, Taiwan.ORCID 0000-0001-6467-8716
China Medical University · TWAsia University · TWE-Da Hospital · TWNational Chung Hsing University · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lapatinib, a dual EGFR/HER2 tyrosine kinase inhibitor, has been shown to improve the survival rate of patients with advanced HER2-positive breast cancers. However, the off-target activity of lapatinib in inducing EGFR expression without tyrosine kinase activity was demonstrated to render HER2-negative breast cancer cells more metastatic, suggesting a limitation to the therapeutic effectiveness of this dual inhibitor in HER2-heterogeneous tumors. Therefore, targeting EGFR expression may be a feasible approach to improve the anticancer efficiency of lapatinib-based therapy. Inhibition of HDAC has been previously reported to epigenetically suppress EGFR protein expression. In this study, however, our data indicated that treatment with HDAC inhibitors trichostatin A (TSA), but not suberoylanilide hydroxamic acid (SAHA) or HDAC siRNA, can attenuate both protein and mRNA expressions of EGFR in lapatinib-treated triple-negative breast cancer cells, suggesting that TSA may suppress EGFR expression independently of HDAC inhibition. Nevertheless, TSA reduced EGFR 3'UTR activity and induced the gene expression of microRNA-7, a known EGFR-targeting microRNA. Furthermore, treatment with microRNA-7 inhibitor attenuated TSA-mediated EGFR suppression. These results suggest that TSA induced microRNA-7 expression to downregulate EGFR expression in an HDAC-independent manner.

Indexed as

Antineoplastic AgentsCell Line, TumorErbB ReceptorsGene Expression Regulation, NeoplasticHistone DeacetylasesHumansHydroxamic AcidsLapatinibMicroRNAsProtein Kinase InhibitorsQuinazolinesRNA, MessengerTriple Negative Breast NeoplasmsAntineoplastic AgentsEGFR protein, humanErbB ReceptorsHistone DeacetylasesHydroxamic AcidsLapatinibMicroRNAsMIRN7-1 microRNA, humanProtein Kinase InhibitorsQuinazolinesRNA, Messengertrichostatin A

Identifiers

PMID24707474
PMCPMC3950925
OpenAlexW2059573980

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.