Evidence map›Paper›PMID 32788343›Full record

ArticleMolecular & cellular proteomics : MCP2020

Multiomics Reveals Ectopic ATP Synthase Blockade Induces Cancer Cell Death via a lncRNA-mediated Phospho-signaling Network.

Yi-Wen Chang, Chia-Lang Hsu, Cheng-Wei Tang, Xiang-Jun Chen, Hsuan-Cheng Huang, Hsueh-Fen Juan

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

12 citing papers in PubMed, 14 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

6 authors at 2 institutions in 1 country.

Yi-Wen ChangDepartment of Life Science, Institute of Molecular and Cellular Biology, National Taiwan University, Taipei, Taiwan.
Chia-Lang HsuDepartment of Life Science, Institute of Molecular and Cellular Biology, National Taiwan University, Taipei, Taiwan; Department of Medical Research, National Taiwan University Hospital, Taipei, Taiwan.
Cheng-Wei TangDepartment of Life Science, Institute of Molecular and Cellular Biology, National Taiwan University, Taipei, Taiwan.
Xiang-Jun ChenDepartment of Life Science, Institute of Molecular and Cellular Biology, National Taiwan University, Taipei, Taiwan.
Hsuan-Cheng HuangInstitute of Biomedical Informatics, National Yang-Ming University, Taipei, Taiwan. Electronic address: hsuancheng@ym.edu.tw.
Hsueh-Fen JuanDepartment of Life Science, Institute of Molecular and Cellular Biology, National Taiwan University, Taipei, Taiwan; Graduate Institute of Biomedical Electronics and Bioinformatics, National Taiwan University, Taipei, Taiwan. Electronic address: yukijuan@ntu.edu.tw.
National Taiwan University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The EGFR tyrosine kinase inhibitor gefitinib is commonly used for lung cancer patients. However, some patients eventually become resistant to gefitinib and develop progressive disease. Here, we indicate that ecto-ATP synthase, which ectopically translocated from mitochondrial inner membrane to plasma membrane, is considered as a potential therapeutic target for drug-resistant cells. Quantitative multi-omics profiling reveals that ecto-ATP synthase inhibitor mediates CK2-dependent phosphorylation of DNA topoisomerase IIα (topo IIα) at serine 1106 and subsequently increases the expression of long noncoding RNA, GAS5. Additionally, we also determine that downstream of GAS5, p53 pathway, is activated by ecto-ATP synthase inhibitor for regulation of programed cell death. Interestingly, GAS5-proteins interactomic profiling elucidates that GAS5 associates with topo IIα and subsequently enhancing the phosphorylation level of topo IIα. Taken together, our findings suggest that ecto-ATP synthase blockade is an effective therapeutic strategy via regulation of CK2/phospho-topo IIα/GAS5 network in gefitinib-resistant lung cancer cells.

Indexed as

Antineoplastic AgentsApoptosisATP Synthetase ComplexesCarcinoma, Non-Small-Cell LungCasein Kinase IICell Line, TumorCell MembraneCell ProliferationCell SurvivalDNA Topoisomerases, Type IIDrug Resistance, NeoplasmGefitinibGene OntologyHumansImmunohistochemistryLung NeoplasmsAntineoplastic AgentsATP Synthetase ComplexesCasein Kinase IIDNA Topoisomerases, Type IIGAS5 long non-coding RNA, humanGefitinibProtein Kinase InhibitorsRNA, Long NoncodingRNA, Small InterferingTP53 protein, humanTumor Suppressor Protein p53cancer therapeuticsdrug resistanceectopic ATP synthasegefitinib resistancelung cancermicro arraysMultiomicsphosphoproteomephosphoproteomicsRNA-binding proteomicstargeted therapiestranscriptional regulation

Identifiers

PMID32788343
PMCPMC7664121
OpenAlexW3048765587

What OpenQuestion holds

Textmetadata
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.