Evidence map›Paper›PMID 29902340›Full record

ArticleCancer science2018

Autophagy inhibition synergizes with calcium mobilization to achieve efficient therapy of malignant gliomas.

Ha Thi Vu, Masahiko Kobayashi, Ahmed M Hegazy, Yuko Tadokoro, Masaya Ueno, Atsuko Kasahara, Yusuke Takase, Naho Nomura, Hui Peng, Chiaki Ito and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

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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

14 authors at 2 institutions in 1 country.

Ha Thi VuCancer and Stem Cell Research Program, Division of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.
Masahiko KobayashiCancer and Stem Cell Research Program, Division of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.
Ahmed M HegazyCancer and Stem Cell Research Program, Division of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.
Yuko TadokoroCancer and Stem Cell Research Program, Division of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.
Masaya UenoCancer and Stem Cell Research Program, Division of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.
Atsuko KasaharaCancer and Stem Cell Research Program, Division of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.
Yusuke TakaseCancer and Stem Cell Research Program, Division of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.
Naho NomuraCancer and Stem Cell Research Program, Division of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.
Hui PengCancer and Stem Cell Research Program, Division of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.
Chiaki ItoCancer and Stem Cell Research Program, Division of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.
Yasushi InoDivision of Innovative Cancer Therapy, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Tomoki TodoDivision of Innovative Cancer Therapy, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Mitsutoshi NakadaDepartment of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa, Japan.
Atsushi HiraoCancer and Stem Cell Research Program, Division of Molecular Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.ORCID http://orcid.org/0000-0001-7818-8240
Kanazawa University · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy plays a critical role in tumorigenesis, but how autophagy contributes to cancer cells' responses to chemotherapeutics remains controversial. To investigate the roles of autophagy in malignant gliomas, we used CRISPR/CAS9 to knock out the ATG5 gene, which is essential for autophagosome formation, in tumor cells derived from patients with glioblastoma. While ATG5 disruption inhibited autophagy, it did not change the phenotypes of glioma cells and did not alter their sensitivity to temozolomide, an agent used for glioblastoma patient therapy. Screening of an anticancer drug library identified compounds that showed greater efficacy to ATG5-knockout glioma cells compared to control. While several selected compounds, including nigericin and salinomycin, remarkably induced autophagy, potent autophagy inducers by mTOR inhibition did not exhibit the ATG5-dependent cytoprotective effects. Nigericin in combination with ATG5 deficiency synergistically suppressed spheroid formation by glioma cells in a manner mitigated by Ca

Indexed as

AnimalsApoptosisAutophagyAutophagy-Related Protein 5CalciumCell Line, TumorChloroquineDacarbazineFemaleGlioblastomaGliomaHumansMiceMice, Inbred BALB CMice, NudeMitochondriaAutophagy-Related Protein 5CalciumChloroquineDacarbazineReactive Oxygen SpeciesTemozolomideautophagycalcium signalingdrug screeningglioblastomamitochondria

Identifiers

PMID29902340
PMCPMC6113445
OpenAlexW2808583639

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.