Evidence map›Paper›PMID 34671205›Full record

ArticleInternational journal of biological sciences2021

Up-regulation of MELK by E2F1 promotes the proliferation in cervical cancer cells.

Hongzhi Sun, Hongmei Ma, Hao Zhang, Minjun Ji

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

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  12. 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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  18. The Functional Role and Regulatory Mechanism of FTO mInternational journal of molecular sciences · 2023
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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

4 authors at 1 institution in 1 country.

Hongzhi SunDepartment of Orthopaedics, Nanjing Jiangbei Hospital affiliated to Nantong University, Nanjing, Jiangsu, 210048, China.
Hongmei MaDepartment of Obstetrics and Gynecology, Ma'anshan People's Hospital, Ma'anshan, Anhui, 243000, China.
Hao ZhangState Key Laboratory of Reproductive Medicine, Department of Histology and Embryology, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Minjun JiDepartment of Pathogen Biology, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cervical cancer is a common gynecologic cancer and a frequent cause of death. In this study, we investigated the role of MELK (maternal embryonic leucine zipper kinase) in cervical cancer. We found that HPV 18 E6/E7 promoted MELK expression by activating E2F1. MELK knockdown blocked cancer cells growth. Furthermore, we used MELK-8A to inhibit the kinase activity of MELK and caused the G2/M phase arrest of cancer cells. Under the treatment of inhibitors, Hela cells formed multipolar spindles and eventually underwent apoptosis. We also found that MELK is involved in protein translation and folding during cell division through the MELK interactome and the temporal proteomic analysis under inhibition with MELK-8A. Altogether, these results suggest that MELK may play a vital role in cancer cell proliferation and indicate a potential therapeutic target for cervical cancer.

Indexed as

Cell ProliferationUp-RegulationAnimalsApoptosisCell DivisionCell Line, TumorE2F1 Transcription FactorFemaleG2 PhaseHumansMass SpectrometryMiceMice, NudeMitosisProtein BindingProtein Serine-Threonine KinasesE2F1 protein, humanE2F1 Transcription FactorMELK protein, humanProtein Serine-Threonine KinasesCell arrestE2F1HPV E6/E7MELKMELK-8APolyploidy

Identifiers

PMID34671205
PMCPMC8495384
OpenAlexW3207786979

What OpenQuestion holds

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LicenceCC BY
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.