Evidence map›Paper›PMID 31821699›Full record

ArticleJournal of cellular and molecular medicine2020

Inhibition of MELK produces potential anti-tumour effects in bladder cancer by inducing G1/S cell cycle arrest via the ATM/CHK2/p53 pathway.

Song Chen, Qiang Zhou, Zicheng Guo, Yejinpeng Wang, Lu Wang, Xuefeng Liu, Mengxin Lu, Lingao Ju, Yu Xiao, Xinghuan Wang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  6. Targeting MELK in tumor cells and tumor microenvironment: from function and mechanism to therapeutic application.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
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  14. Corrigendum.Journal of cellular and molecular medicine · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Song ChenDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Qiang ZhouDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Zicheng GuoDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Yejinpeng WangDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Lu WangDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Xuefeng LiuDepartment of Pathology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Mengxin LuDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Lingao JuDepartment of Biological Repositories, Zhongnan Hospital of Wuhan University, Wuhan, China.
Yu XiaoDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.ORCID 0000-0003-1377-9685
Xinghuan WangDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.ORCID 0000-0003-3497-0024
Wuhan University · CNGeorgetown University · USQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We aimed to investigate the biological function of MELK and the therapeutic potential of OTSSP167 in human bladder cancer (BCa). First, we observed overexpression of MELK in BCa cell lines and tissues and found that it was associated with higher tumour stage and tumour grade, which was consistent with transcriptome analysis. High expression of MELK was significantly correlated with poor prognosis in BCa patients, and MELK was found to have a role in the cell cycle, the G1/S transition in mitosis, and DNA repair and replication. Furthermore, BCa cells presented significantly decreased proliferation capacity following silencing of MELK or treatment with OTSSP167 in vitro and in vivo. Functionally, reduction in MELK or treatment of cells with OTSSP167 could induce cell cycle arrest and could suppress migration. In addition, these treatments could activate phosphorylation of ATM and CHK2, which would be accompanied by down-regulated MDMX, cyclin D1, CDK2 and E2F1; however, p53 and p21 would be activated. Opposite results were observed when MELK expression was induced. Overall, MELK was found to be a novel oncogene in BCa that induces cell cycle arrest via the ATM/CHK2/p53 pathway. OTSSP167 displays potent anti-tumour activities, which may provide a new molecule-based strategy for BCa treatment.

Indexed as

Cell Cycle CheckpointsAgedAnimalsAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsCell Line, TumorCell MovementCell ProliferationCheckpoint Kinase 2Disease ProgressionFemaleGene Expression Regulation, NeoplasticGene SilencingHumansMaleMice, Inbred BALB C1-(6-(3,5-dichloro-4-hydroxyphenyl)-4-((4-((dimethylamino)methyl)cyclohexyl)amino)-1,5-naphthyridin-3-yl)ethanoneAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsCheckpoint Kinase 2CHEK2 protein, humanMELK protein, humanNaphthyridinesProtein Serine-Threonine KinasesRNA, MessengerTumor Suppressor Protein p53bladder cancercell cycleMELKOTSSP167p53

Identifiers

PMID31821699
PMCPMC6991658
OpenAlexW2994928858

What OpenQuestion holds

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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.