Evidence map›Paper›PMID 32869317›Full record

ArticleJournal of cellular physiology2021

Phospholipase D1 is upregulated by vorinostat and confers resistance to vorinostat in glioblastoma.

Dong Woo Kang, Won Chan Hwang, Yu Na Noh, Youra Kang, Younghoon Jang, Jung-Ae Kim, Do Sik Min

Open access · hybridAbstract read
In one paragraph

Article in Journal of cellular physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Unraveling the role of specificity protein 1 in gliomas: pathophysiology and clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  11. Biomaterial-basedCancer pathogenesis and therapy · 2023
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  14. The contributing factors of resistance or sensitivity to epigenetic drugs in the treatment of AML.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  15. Programmed cell death, redox imbalance, and cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2021
    Review
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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

7 authors at 5 institutions in 1 country.

Dong Woo KangDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan, Republic of Korea.
Won Chan HwangDepartment of Molecular Biology, College of Natural Science, Pusan National University, Busan, Republic of Korea.
Yu Na NohInstitute for Innovative Cancer Research, Biomedical Research Center, Asan Medical Center, Seoul, Republic of Korea.
Youra KangCollege of Pharmacy, Yeungnam University, Gyeongsan, South Korea.
Younghoon JangDepartment of Biology and Chemistry, Changwon National University, Changwon, Korea.
Jung-Ae KimCollege of Pharmacy, Yeungnam University, Gyeongsan, South Korea.
Do Sik MinCollege of Pharmacy, Yonsei University, Incheon, South Korea.ORCID 0000-0002-8570-5098
Yeungnam University · KRYonsei University · KRAsan Medical Center · KRChangwon National University · KRPusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is an aggressive brain tumor and drug resistance remains a major barrier for therapeutics. Epigenetic alterations are implicated in GBM pathogenesis, and epigenetic modulators including histone deacetylase (HDAC) inhibitors are exploited as promising anticancer therapies. Here, we demonstrate that phospholipase D1 (PLD1) is a transcriptional target of HDAC inhibitors and confers resistance to HDAC inhibitor in GBM. Treatment of vorinostat upregulates PLD1 through PKCζ-Sp1 axis. Vorinostat induces dynamic changes in the chromatin structure and transcriptional machinery associated with PLD1 promoter region. Cotreatment of vorinostat with PLD1 inhibitor further attenuates invasion, angiogenesis, colony-forming capacity, and self-renewal capacity, compared with those of either treatment. PLD1 inhibitor overcomes resistance to vorinostat in GBM cells intracranial GBM tumors. Our finding provides new insight into the role of PLD1 as a target of resistance to vorinostat, and PLD1 inhibitor might provide the basis for therapeutic combinations with improved efficacy of HDAC inhibitor.

Indexed as

AnimalsAntineoplastic AgentsBrain NeoplasmsCell Line, TumorChromatinDrug Resistance, NeoplasmEpigenomicsGlioblastomaHistone Deacetylase InhibitorsHumansMiceMice, Inbred C57BLMice, NudeNeovascularization, PathologicPhospholipase DPromoter Regions, GeneticAntineoplastic AgentsChromatinHistone Deacetylase InhibitorsPhospholipase Dphospholipase D1VorinostatglioblastomaHDAC inhibitorphospholipase D1resistancetumorigenesis

Identifiers

PMID32869317
PMCPMC7692931
OpenAlexW3082344753

What OpenQuestion holds

Textmetadata
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.