Evidence map›Paper›PMID 38247322›Full record

ArticleAnimal models and experimental medicine2024

Aurora B facilitates cholangiocarcinoma progression by stabilizing c-Myc.

Ke Liu, Xuxuan Zhou, Fei Huang, Lihao Liu, Zijian Xu, Chongqing Gao, Keke Zhang, Jian Hong, Nan Yao, Guohua Cheng

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

Article in Animal models and experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Ke LiuCollege of Pharmacy, Jinan University, Guangzhou, China.
Xuxuan ZhouDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, China.
Fei HuangCollege of Pharmacy, Jinan University, Guangzhou, China.
Lihao LiuSchool of Medicine, Jinan University, Guangzhou, China.
Zijian XuSchool of Medicine, Jinan University, Guangzhou, China.
Chongqing GaoDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, China.
Keke ZhangDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, China.
Jian HongDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, China.
Nan YaoDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, China.
Guohua ChengCollege of Pharmacy, Jinan University, Guangzhou, China.ORCID 0009-0008-0261-4782
Jinan University · CN

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2023A1515011892National Natural Science Foundation of China 82172602
6 · The paper itself

Abstract

backgroundCholangiocarcinoma (CCA), a malignancy that arises from biliary epithelial cells, has a dismal prognosis, and few targeted therapies are available. Aurora B, a key mitotic regulator, has been reported to be involved in the progression of various tumors, yet its role in CCA is still unclarified.

methodsHuman CCA tissues and murine spontaneous CCA models were used to assess Aurora B expression in CCA. A loss-of-function model was constructed in CCA cells to determine the role of Aurora B in CCA progression. Subcutaneous and liver orthotopic xenograft models were used to assess the therapeutic potential of Aurora B inhibitors in CCA.

resultsIn murine spontaneous CCA models, Aurora B was significantly upregulated. Elevated Aurora B expression was also observed in 62.3% of human specimens in our validation cohort (143 CCA specimens), and high Aurora B expression was positively correlated with pathological parameters of tumors and poor survival. Knockdown of Aurora B by siRNA and heteroduplex oligonucleotide (HDO) or an Aurora B kinase inhibitor (AZD1152) significantly suppressed CCA progression via G2/M arrest induction. An interaction between Aurora B and c-Myc was found in CCA cells. Targeting Aurora B significantly reduced this interaction and accelerated the proteasomal degradation of c-Myc, suggesting that Aurora B promoted the malignant properties of CCA by stabilizing c-Myc. Furthermore, sequential application of AZD1152 or Aurora B HDO drastically improved the efficacy of gemcitabine in CCA.

conclusionsAurora B plays an essential role in CCA progression by modulating c-Myc stability and represents a new target for treatment and chemosensitization in CCA.

Indexed as

Aurora Kinase BBile Duct NeoplasmsCholangiocarcinomaDisease ProgressionProto-Oncogene Proteins c-mycAnimalsCell Line, TumorFemaleGemcitabineHumansMaleMiceMice, NudeOrganophosphatesQuinazolines2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphateAURKB protein, humanAurora Kinase BGemcitabineOrganophosphatesProto-Oncogene Proteins c-mycQuinazolinesAurora B kinaseCholangiocarcinomac‐Myccombination therapytargeted therapy

Identifiers

PMID38247322
PMCPMC11528393
OpenAlexW4391107673

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.