Evidence map›Paper›PMID 32943609›Full record

ArticleCell death & disease2020

Wnt/β-catenin signaling pathway induces autophagy-mediated temozolomide-resistance in human glioblastoma.

Eun-Jin Yun, Sangwoo Kim, Jer-Tsong Hsieh, Seung Tae Baek

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
11.5field-weighted citation impact, top 1% 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

76 citing papers in PubMed, 121 citations in OpenAlex.

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  5. Biomedicines · 2026
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16 more citing papers are in PubMed but not listed here.

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 3 institutions in 3 countries.

Eun-Jin Yun *POSTECH Biotech Center, POSTECH, Pohang, Republic of Korea. ejyun@postech.ac.kr.ORCID http://orcid.org/0000-0002-4454-7150
Sangwoo KimDepartment of Biomedical Systems Informatics and Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jer-Tsong HsiehDepartment of Urology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Seung Tae Baek *Institute for Convergence Research and Education in Advanced Technology, Yonsei University, Seoul, Republic of Korea. sbaek@postech.ac.kr.ORCID http://orcid.org/0000-0003-0040-1501
Pohang University of Science and Technology · KRKaohsiung Medical University · TWYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Temozolomide (TMZ) is widely used for treating glioblastoma multiforme (GBM), however, the treatment of such brain tumors remains a challenge due to the development of resistance. Increasing studies have found that TMZ treatment could induce autophagy that may link to therapeutic resistance in GBM, but, the precise mechanisms are not fully understood. Understanding the molecular mechanisms underlying the response of GBM to chemotherapy is paramount for developing improved cancer therapeutics. In this study, we demonstrated that the loss of DOC-2/DAB2 interacting protein (DAB2IP) is responsible for TMZ-resistance in GBM through ATG9B. DAB2IP sensitized GBM to TMZ and suppressed TMZ-induced autophagy by negatively regulating ATG9B expression. A higher level of ATG9B expression was associated with GBM compared to low-grade glioma. The knockdown of ATG9B expression in GBM cells suppressed TMZ-induced autophagy as well as TMZ-resistance. Furthermore, we showed that DAB2IP negatively regulated ATG9B expression by blocking the Wnt/β-catenin pathway. To enhance the benefit of TMZ and avoid therapeutic resistance, effective combination strategies were tested using a small molecule inhibitor blocking the Wnt/β-catenin pathway in addition to TMZ. The combination treatment synergistically enhanced the efficacy of TMZ in GBM cells. In conclusion, the present study identified the mechanisms of TMZ-resistance of GBM mediated by DAB2IP and ATG9B which provides insight into a potential strategy to overcome TMZ chemo-resistance.

Indexed as

AutophagyDrug Resistance, NeoplasmAntineoplastic Agents, AlkylatingAutophagy-Related Proteinsbeta CateninCell Line, TumorCentral Nervous System NeoplasmsDown-RegulationGene Expression Regulation, NeoplasticGlioblastomaHumansInhibitory Concentration 50Membrane ProteinsMicroRNAsras GTPase-Activating ProteinsSignal TransductionAntineoplastic Agents, AlkylatingATG9B protein, humanAutophagy-Related Proteinsbeta CateninDAB2IP protein, humanMembrane ProteinsMicroRNAsras GTPase-Activating ProteinsTemozolomideWnt Proteins

Identifiers

PMID32943609
PMCPMC7498596
OpenAlexW3087640434

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.