Evidence map›Paper›PMID 29163769›Full record

ArticleOncotarget2017

YAP1 is essential for tumor growth and is a potential therapeutic target for EGFR-dependent lung adenocarcinomas.

Ting-Fang Lee, Yu-Chi Tseng, Wei-Chin Chang, Yi-Chen Chen, Yu-Rung Kao, Teh-Ying Chou, Chao-Chi Ho, Cheng-Wen Wu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 21 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

8 authors at 5 institutions in 1 country.

Ting-Fang LeeInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Yu-Chi TsengInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan.
Wei-Chin ChangInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Yi-Chen ChenInstitute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan.
Yu-Rung KaoInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Teh-Ying ChouInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Chao-Chi HoDepartment of Internal Medicine, National Taiwan University Hospital and National Taiwan University Medical College, Taipei, Taiwan.
Cheng-Wen WuInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Institute of Molecular Biology, Academia Sinica · TWNational Yang Ming Chiao Tung University · TWInstitute of Biomedical Sciences, Academia Sinica · TWMackay Memorial Hospital · TWNational Taiwan University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) mutations are found in lung adenocarcinomas leading to tumor cells proliferation and survival. EGFR tyrosine kinase inhibitors (TKIs) that block EGFR activity are effective therapeutics for EGFR-mutant lung adenocarcinoma patients, but TKI-resistance inevitably occurs. The YES-associated protein (YAP1) transcription coactivator has been implicated as an oncogene and is amplified in human cancers and provides tumor cells strong proliferation and survival cues. This study investigated the roles of YAP1 in lung adenocarcinoma by exploring its regulation and functions mediated by EGFR signaling. In this study, we detected a correlation between YAP1 level and EGFR mutation status in lung adenocarcinoma tissues. Using lung adenocarcinoma cell lines, enhanced YAP1 expression and activity mediated by EGFR signaling was detected through enhanced protein stability. A SRC family protein, YES, was involved in EGFR-regulated YAP1 expression and this pathway was crucial for proliferation in EGFR-dependent cells. Small molecules that reduced YAP1 levels by mechanisms bypassing EGFR signaling were effective in reducing viability in EGFR-dependent cells including those with EGFR T790M, the major cause of TKI-resistance. These observations unveiled the significance of YAP1 in EGFR mutant lung adenocarcinomas and identified YAP1 as a promising therapeutic target for EGFR-dependent lung adenocarcinoma patients, including those with EGFR T790M-caused TKI resistance.

Indexed as

EGFR mutationlung adenocarcinomaTKI-resistanceYAP1

Identifiers

PMID29163769
PMCPMC5685690
OpenAlexW2741451060

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.