Evidence map›Paper›PMID 37537339›Full record

ArticleNPJ precision oncology2023

HER3 targeting augments the efficacy of panobinostat in claudin-low triple-negative breast cancer cells.

Hui Lyu, Defu Hou, Hao Liu, Sanbao Ruan, Congcong Tan, Jiande Wu, Chindo Hicks, Bolin Liu

Open access · goldAbstract read
In one paragraph

Article in NPJ precision oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
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  6. Histone Deacetylase 6 (HDAC6) in Ciliopathies: Emerging Insights and Therapeutic Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  7. 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

8 authors at 2 institutions in 2 countries.

Hui LyuDepartments of Interdisciplinary Oncology, Louisiana State University (LSU) Health Sciences Center, New Orleans, LA, USA. hlyu@lsuhsc.edu.ORCID http://orcid.org/0000-0003-1851-2533
Defu HouDepartments of Interdisciplinary Oncology, Louisiana State University (LSU) Health Sciences Center, New Orleans, LA, USA.
Hao LiuDepartments of Interdisciplinary Oncology, Louisiana State University (LSU) Health Sciences Center, New Orleans, LA, USA.
Sanbao RuanDepartments of Interdisciplinary Oncology, Louisiana State University (LSU) Health Sciences Center, New Orleans, LA, USA.
Congcong TanDepartments of Interdisciplinary Oncology, Louisiana State University (LSU) Health Sciences Center, New Orleans, LA, USA.
Jiande WuDepartments of Genetics, Stanley S. Scott Cancer Center, School of Medicine, Louisiana State University (LSU) Health Sciences Center, New Orleans, LA, USA.
Chindo HicksDepartments of Genetics, Stanley S. Scott Cancer Center, School of Medicine, Louisiana State University (LSU) Health Sciences Center, New Orleans, LA, USA.
Bolin LiuDepartments of Interdisciplinary Oncology, Louisiana State University (LSU) Health Sciences Center, New Orleans, LA, USA. bliu2@lsuhsc.edu.ORCID http://orcid.org/0000-0003-0150-8650
Louisiana State University Health Sciences Center New Orleans · USHunan Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with triple-negative breast cancer (TNBC) have a poor prognosis and high relapse rate due to limited therapeutic options. This study was conducted to determine the mechanisms of action of panobinostat, a pan-inhibitor of histone deacetylase (HDAC) and FDA-approved medication for multiple myeloma, in TNBC and to provide a rationale for effective drug combinations against this aggressive disease. RNA sequencing analyses of the claudin-low (CL) TNBC (MDA-MB-231) cells untreated or treated with panobinostat were performed to identify the differentially expressed genes. Adaptive alterations in gene expression were analyzed and validated in additional CL TNBC cells. Tumor xenograft models were used to test the in vivo antitumor activity of panobinostat alone or its combinations with gefitinib, an EGFR-tyrosine kinase inhibitor (TKI). Panobinostat potently inhibited proliferation and induced apoptosis in all TNBC cells tested. However, in CL TNBC cells, this HDAC inhibitor markedly enhanced expression of HER3, which interacted with EGFR to activate both receptors and Akt signaling pathways. Combinations of panobinostat and gefitinib synergistically suppressed CL TNBC cell proliferation and promoted apoptosis in vitro and in vivo. Upregulation of HER3 compromises the efficacy of panobinostat in CL TNBC. Inactivation of HER3 combined with panobinostat represents a practical approach to combat CL TNBC.

Identifiers

PMID37537339
PMCPMC10400567
OpenAlexW4385550887

What OpenQuestion holds

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LicenceCC BY
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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.