Evidence map›Paper›PMID 28286419›Full record

ArticleCancer cell international2017

Dual roles of extracellular signal-regulated kinase (ERK) in quinoline compound BPIQ-induced apoptosis and anti-migration of human non-small cell lung cancer cells.

Yao Fong, Chang-Yi Wu, Kuo-Feng Chang, Bing-Hung Chen, Wan-Ju Chou, Chih-Hua Tseng, Yen-Chun Chen, Hui-Min David Wang, Yeh-Long Chen, Chien-Chih Chiu

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

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  12. A brief overview of antitumoral actions of bruceine D.Exploration of targeted anti-tumor therapy · 2020
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  15. Cancer cell international · 2018
    Article
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

10 authors at 4 institutions in 1 country.

Yao Fong *Department of Thoracic Surgery, Chi-Mei Medical Center, Tainan, 710 Taiwan.
Chang-Yi Wu *Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung, 804 Taiwan.
Kuo-Feng ChangDepartment of Biotechnology, Kaohsiung Medical University, Kaohsiung, 807 Taiwan.
Bing-Hung ChenDepartment of Biotechnology, Kaohsiung Medical University, Kaohsiung, 807 Taiwan.
Wan-Ju ChouDepartment of Biotechnology, Kaohsiung Medical University, Kaohsiung, 807 Taiwan.
Chih-Hua TsengSchool of Pharmacy, Kaohsiung Medical University, Kaohsiung, 807 Taiwan.
Yen-Chun ChenDepartment of Biotechnology, Kaohsiung Medical University, Kaohsiung, 807 Taiwan.
Hui-Min David WangGraduate Institute of Biomedical Engineering, National Chung Hsing University, Taichung, 402 Taiwan.
Yeh-Long ChenDepartment of Medicinal and Applied Chemistry, Kaohsiung Medical University, Kaohsiung, 807 Taiwan.
Chien-Chih ChiuDepartment of Biological Sciences, National Sun Yat-sen University, Kaohsiung, 804 Taiwan.
Kaohsiung Medical University · TWNational Sun Yat-sen University · TWChi Mei Medical Center · TWNational Chung Hsing University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background2,9-Bis[2-(pyrrolidin-1-yl)ethoxy]-6-{4-[2-(pyrrolidin-1-yl)ethoxy] phenyl}-11

methodsWestern Blot assay was performed for detecting the activation of MAPK members in NSCLC H1299 cells following BPIQ administration. Cellular proliferation was determined using a trypan blue exclusion assay. Cellular apoptosis was detected using flow cytometer-based Annexin V/propidium iodide dual staining. Cellular migration was determined using wound-healing assay and Boyden's chamber assay. Zymography assay was performed for examining MMP-2 and -9 activities. The assessment of MAPK inhibition was performed for further validating the role of JNK, p38, and ERK in BPIQ-induced growth inhibition, apoptosis, and migration of NSCLC cells.

resultsWestern Blot assay showed that BPIQ treatment upregulates the phosphorylated levels of both MAPK proteins JNK and ERK. However, only ERK inhibitor rescues BPIQ-induced growth inhibition of NSCLC H1299 cells. The results of Annexin V assay further confirmed the pro-apoptotic role of ERK in BPIQ-induced cell death of H1299 cells. The results of wound healing and Boyden chamber assays showed that sub-IC

conclusionsOur results suggest ERK may play dual roles in BPIQ-induced apoptosis and anti-migration, and it would be worthwhile further developing strategies for treating chemoresistant lung cancers through modulating ERK activity.

Indexed as

ApoptosisBPIQCellular migrationERKIndeno[1,2-c]quinolineLung cancerMAPKQuinoline

Identifiers

PMID28286419
PMCPMC5339964
OpenAlexW2593137377

What OpenQuestion holds

Textmetadata
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.