Evidence map›Paper›PMID 33176854›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

Loss of PLK2 induces acquired resistance to temozolomide in GBM via activation of notch signaling.

Wahafu Alafate, Dongze Xu, Wei Wu, Jianyang Xiang, Xudong Ma, Wanfu Xie, Xiaobin Bai, Maode Wang, Jia Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. 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
2.7field-weighted citation impact, top 9% 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, 33 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Polo-like kinase2 regulates renal tubulointerstitial fibrosis via notch signaling pathway in diabetic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  7. Review
  8. Article
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  11. Article
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  16. Disease markers · 2022
    Article
  17. Small Interfering RNA for Gliomas Treatment: Overcoming Hurdles in Delivery.Frontiers in cell and developmental biology · 2022
    Review
  18. Review
  19. Hippo Pathway in Regulating Drug Resistance of Glioblastoma.International journal of molecular sciences · 2021
    Review
  20. Review
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

9 authors at 1 institution in 1 country.

Wahafu AlafateDepartment of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, P.R. China.
Dongze XuDepartment of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, P.R. China.
Wei WuDepartment of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, P.R. China.
Jianyang XiangDepartment of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, P.R. China.
Xudong MaDepartment of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, P.R. China.
Wanfu XieDepartment of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, P.R. China.
Xiaobin BaiDepartment of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, P.R. China.
Maode WangDepartment of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, P.R. China. maodewang@163.com.
Jia WangDepartment of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, P.R. China. jiawang_xjtu@163.com.
First Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

Fundamental Research Funds of Xi'an Jiaotong University no. 1191329177Natural Science Foundation of Shaanxi Province no. 2019JQ-958Young Scientists Fund 81802502
6 · The paper itself

Abstract

backgroundGlioblastoma (GBM) is a lethal type of primary brain tumor with a median survival less than 15 months. Despite the recent improvements of comprehensive strategies, the outcomes for GBM patients remain dismal. Accumulating evidence indicates that rapid acquired chemoresistance is the major cause of GBM recurrence thus leads to worse clinical outcomes. Therefore, developing novel biomarkers and therapeutic targets for chemoresistant GBM is crucial for long-term cures.

methodsTranscriptomic profiles of glioblastoma were downloaded from gene expression omnibus (GEO) and TCGA database. Differentially expressed genes were analyzed and candidate gene PLK2 was selected for subsequent validation. Clinical samples and corresponding data were collected from our center and measured using immunohistochemistry analysis. Lentiviral transduction and in vivo xenograft transplantation were used to validate the bioinformatic findings. GSEA analyses were conducted to identify potential signaling pathways related to PLK2 expression and further confirmed by in vitro mechanistic assays.

resultsIn this study, we identified PLK2 as an extremely suppressed kinase-encoding gene in GBM samples, particularly in therapy resistant GBM. Additionally, reduced PLK2 expression implied poor prognosis and TMZ resistance in GBM patients. Functionally, up-regulated PLK2 attenuated cell proliferation, migration, invasion, and tumorigenesis of GBM cells. Besides, exogenous overexpression of PLK2 reduced acquired TMZ resistance of GBM cells. Furthermore, bioinformatics analysis indicated that PLK2 was negatively correlated with Notch signaling pathway in GBM. Mechanically, loss of PLK2 activated Notch pathway through negative transcriptional regulation of HES1 and degradation of Notch1.

conclusionLoss of PLK2 enhances aggressive biological behavior of GBM through activation of Notch signaling, indicating that PLK2 could be a prognostic biomarker and potential therapeutic target for chemoresistant GBM.

Indexed as

AnimalsBrain NeoplasmsFemaleGlioblastomaHumansMiceMice, NudeProtein Serine-Threonine KinasesReceptors, NotchSignal TransductionTemozolomideTranscriptomeXenograft Model Antitumor AssaysPLK2 protein, humanProtein Serine-Threonine KinasesReceptors, NotchTemozolomideChemoresistanceGBMNotch signalingPLK2TMZ

Identifiers

PMID33176854
PMCPMC7657349
OpenAlexW3105026771

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.