Evidence map›Paper›PMID 25712415›Full record

ArticleJournal of cellular and molecular medicine2015

17-AAG suppresses growth and invasion of lung adenocarcinoma cells via regulation of the LATS1/YAP pathway.

Xiang-Yun Ye, Qing-Quan Luo, Yun-Hua Xu, Nai-Wang Tang, Xiao-Min Niu, Zi-Ming Li, Sheng-Ping Shen, Shun Lu, Zhi-Wei Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 27 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

9 authors at 2 institutions in 1 country.

Xiang-Yun YeDepartment of Shanghai Lung Tumor Clinical Medical Centre, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Qing-Quan Luo
Yun-Hua Xu
Nai-Wang Tang
Xiao-Min Niu
Zi-Ming Li
Sheng-Ping Shen
Shun Lu
Zhi-Wei Chen
Shanghai Chest Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The large tumour suppressor 1 (LATS1) signalling network has been proved to be an essential regulator within the cell, participating in multiple cellular phenotypes. However, it is unclear concerning the clinical significance of LATS1 and the regulatory mechanisms of 17-Allylamino-17- demethoxygeldanamycin (17-AAG) in lung adenocarcinoma (LAC). The aim of the present study was to investigate the correlation of LATS1 and yes-associated protein (YAP) expression with clinicopathological characteristics in LAC patients, and the effects of 17-AAG on biological behaviours of LAC cells. Subcutaneous LAC tumour models were further established to observe the tumour growth in nude mice. The results showed that the positive expression of LATS1 was significantly lowered (26.7% versus 68.0%, P < 0.001), while that of YAP was elevated (76.0% versus 56.0%, P = 0.03) in LAC tissues compared to the adjacent non-cancerous tissues; LAST1 expression was negatively correlated with YAP expression (r = 0.432, P < 0.001) and lymphatic invasion of the tumour (P = 0.015). In addition, 17-AAG inhibited proliferation and invasion, and induced cell apoptosis and cycle arrest in LAC cells together with increased expression of E-cadherin and p-LATS1, and decreased expression of YAP and connective tissue growth factor. Tumour volumes and weight were much smaller in 17-AAG-treated groups than those in untreated group (P < 0.01). Taken together, our findings indicate that decreased expression of LATS1 is associated with lymphatic invasion of LAC, and 17-AAG suppresses growth and invasion of LAC cells via regulation of the LATS1/YAP pathway in vitro and in vivo, suggesting that we may provide a promising therapeutic strategy for the treatment of human LAC.

Indexed as

Adaptor Proteins, Signal TransducingAdenocarcinomaAdenocarcinoma of LungAnimalsAntineoplastic AgentsApoptosisBenzoquinonesCadherinsCell Cycle CheckpointsCell Line, TumorCell ProliferationConnective Tissue Growth FactorFemaleGene Expression Regulation, NeoplasticHSP90 Heat-Shock ProteinsHumansAdaptor Proteins, Signal TransducingAntineoplastic AgentsBenzoquinonesCadherinsConnective Tissue Growth FactorHSP90 Heat-Shock ProteinsLactams, MacrocyclicLATS1 protein, humanPhosphoproteinsProtein Serine-Threonine KinasestanespimycinTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins17-AAGgrowthinvasionLATS1lung adenocarcinoma

Identifiers

PMID25712415
PMCPMC4369821
OpenAlexW1998590599

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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.