Evidence map›Paper›PMID 39863788›Full record

ArticleScientific reports2025

Proteomic profiling identifies upregulation of aurora kinases causing resistance to taxane-type chemotherapy in triple negative breast cancer.

Bohan Ning, Chang Liu, Ali Cem Kucukdagli, Jiuyi Zhang, Han Jing, Zhiqian Zhou, Yuwei Zhang, Ying Dong, Yunjia Chen, Hua Guo and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Review
  2. Review
  3. Discovery of thieno[2,3-RSC advances · 2026
    Article
  4. Discovery of the first-in-class Aurora B kinase selective degrader.European journal of medicinal chemistry · 2025
    Article
  5. Article
  6. Review
  7. 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

11 authors.

Bohan Ning *Department of Genetics, The University of Alabama at Birmingham, Birmingham, AL, USA.
Chang Liu *Department of Genetics, The University of Alabama at Birmingham, Birmingham, AL, USA.
Ali Cem KucukdagliDepartment of Genetics, The University of Alabama at Birmingham, Birmingham, AL, USA.
Jiuyi ZhangDepartment of Genetics, The University of Alabama at Birmingham, Birmingham, AL, USA.
Han JingDepartment of Genetics, The University of Alabama at Birmingham, Birmingham, AL, USA.
Zhiqian ZhouDepartment of Genetics, The University of Alabama at Birmingham, Birmingham, AL, USA.
Yuwei ZhangDepartment of Genetics, The University of Alabama at Birmingham, Birmingham, AL, USA.
Ying DongDepartment of Pathology, Peking University First Hospital, Beijing, China.
Yunjia ChenDepartment of Genetics, The University of Alabama at Birmingham, Birmingham, AL, USA.
Hua GuoDepartment of Pathology, Heersink School of Medicine, The University of Alabama at Birmingham, 720 20th Street South, Birmingham, AL, 35294, USA. huaguo@uabmc.edu.
Jia XuDepartment of Genetics, The University of Alabama at Birmingham, Birmingham, AL, USA. xuj@uab.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nowadays, chemotherapy and immunotherapy remain the major treatment strategies for Triple-Negative Breast Cancer (TNBC). Identifying biomarkers to pre-select and subclassify TNBC patients with distinct chemotherapy responses is essential. In the current study, we performed an unbiased Reverse Phase Protein Array (RPPA) on TNBC cells treated with chemotherapy compounds and found a leading significant increase of phosphor-AURKA/B/C, AURKA, AURKB, and PLK1, which fall into the mitotic kinase group. The increase of AURKA and AURKB protein was majorly due to a post-transcription level regulation, and Paclitaxel treatment induced Aurora Kinases protein phosphorylation on AURKA(T288)/AURKB(T232) sites and their protein stability. In our UAB TNBC cohort, the expression of AURKA and AURKB was significantly higher in TNBC tumors compared to normal adjacent tissues, and AURKB was found to be highly expressed in African American TNBC patients compared to European Americans. Moreover, Aurora Kinases overexpression in TNBC cells renders resistance to Paclitaxel treatment and attenuates the apoptosis effect triggered by chemotherapy treatment, suggesting Aurora Kinases could mediate the chemo-resistance in TNBC. Hence, a combination of Aurora kinase inhibitors or PROTAC degrader and taxane-type chemotherapy significantly enhanced the chemotherapy effect. In summary, we revealed that Aurora Kinases upregulation after treatment with chemotherapy could confer chemotherapy resistance to TNBC cells, and AURKB could serve as preselection markers for stratifying patients' response to neoadjuvant chemotherapy.

Indexed as

Aurora Kinase AAurora Kinase BAurora KinasesBridged-Ring CompoundsDrug Resistance, NeoplasmProteomicsTaxoidsTriple Negative Breast NeoplasmsApoptosisCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansPaclitaxelPhosphorylationUp-RegulationAURKA protein, humanAURKB protein, humanAurora Kinase AAurora Kinase BAurora KinasesBridged-Ring CompoundsPaclitaxeltaxaneTaxoidsAURKAAURKBCancer DisparityNeoadjuvant ChemotherapyTNBC

Identifiers

PMID39863788
PMCPMC11762698

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.