Evidence map›Paper›PMID 32851091›Full record

ArticleBioMed research international2020

AURKA Increase the Chemosensitivity of Colon Cancer Cells to Oxaliplatin by Inhibiting the TP53-Mediated DNA Damage Response Genes.

Baocong Shan, Ran Zhao, Jian Zhou, Minghui Zhang, Xiaoyu Qi, Tianzhen Wang, Jinan Gong, Yiqi Wu, Yuanyuan Zhu, Weiwei Yang and 3 more

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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  10. Pan-cancer analysis andFrontiers in oncology · 2023
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  12. Identification of Novel Genes and Associated Drugs in Cervical Cancer by Bioinformatics Methods.Medical science monitor : international medical journal of experimental and clinical research · 2022
    Article
  13. Article
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  15. 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

13 authors at 4 institutions in 1 country.

Baocong ShanDepartment of Pathology, Harbin Medical University, Harbin 150081, China.
Ran ZhaoDepartment of Pathology, Harbin Medical University, Harbin 150081, China.
Jian ZhouDepartment of Pathology, Harbin Medical University, Harbin 150081, China.
Minghui ZhangDepartment of Oncology, Chifeng City Hospital, Chifeng 024000, China.
Xiaoyu QiHospital of Stomatology, Zunyi Medical University, Zunyi 563099, China.
Tianzhen WangDepartment of Pathology, Harbin Medical University, Harbin 150081, China.
Jinan GongDepartment of Pathology, Harbin Medical University, Harbin 150081, China.
Yiqi WuDepartment of Pathology, Harbin Medical University, Harbin 150081, China.
Yuanyuan ZhuDepartment of Pathology, Harbin Medical University, Harbin 150081, China.
Weiwei YangDepartment of Pathology, Harbin Medical University, Harbin 150081, China.
Yang ZhangDepartment of Pathology, Shenyang Fourth People's Hospital, Shenyang 110031, China.ORCID https://orcid.org/0000-0002-1046-4752
Guangyou WangDepartment of Neurobiology, Harbin Medical University, Harbin 150081, China.ORCID https://orcid.org/0000-0002-9490-0637
Xiaobo LiDepartment of Pathology, Harbin Medical University, Harbin 150081, China.ORCID https://orcid.org/0000-0003-1037-3903
Harbin Medical University · CNChifeng Municipal Hospital · CNShenyang The Fourth Hospital of People · CNZunyi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AURKA, a cell cycle-regulated kinase, is associated with malignant transformation and progression in many cancer types. We analyzed the expression change of AURKA in pan-cancer and its effect on the prognosis of cancer patients using the TCGA dataset. We revealed that AURKA was extensively elevated and predicted a poor prognosis in most of the detected cancer types, with an exception in colon cancer. AURKA was elevated in colon cancer, but the upregulation of AURKA indicated better outcomes of colon cancer patients. Then we revealed that undermethylation of the AURKA gene and several transcription factors contributed to the upregulation of AURKA in colon cancer. Moreover, we demonstrated that AURKA overexpression promoted the death of colon cancer cells induced by Oxaliplatin, whereas knockdown of AURKA significantly weakened the chemosensitivity of colon cancer cells to Oxaliplatin. Mechanistically, AURKA inhibited DNA damage response by suppressing the expression of various DNA damage repair genes in a TP53-dependent manner, which can partly explain that ARUKA is associated with a beneficial outcome of colon cancer. This study provided a possibility to use AURKA as a biomarker to predict the chemosensitivity of colon cancer to platinum in the clinic.

Indexed as

AnimalsAurora Kinase AColonic NeoplasmsDNA DamageDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHCT116 CellsHumansMiceOxaliplatinTumor Suppressor Protein p53Xenograft Model Antitumor AssaysAURKA protein, humanAurora Kinase AOxaliplatinTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID32851091
PMCPMC7439175
OpenAlexW3048762836

What OpenQuestion holds

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LicenceCC BY
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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.