Evidence map›Paper›PMID 35116735›Full record

ArticleTranslational cancer research2019

Akt/mTOR and AMPK signaling pathways are responsible for liver X receptor agonist GW3965-enhanced gefitinib sensitivity in non-small cell lung cancer cell lines.

Qingbo Wang, Bo Shen, Xiaobing Qin, Siwen Liu, Jifeng Feng

Open access · diamondAbstract read
In one paragraph

Article in Translational cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 17 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

5 authors at 2 institutions in 1 country.

Qingbo WangThe Fourth Clinical School of Nanjing Medical University, Nanjing 210029, China.
Bo ShenDepartment of Chemotherapy, Nanjing Medical University Affiliated Cancer Hospital Cancer Institute of Jiangsu Province, Nanjing 210009, China.
Xiaobing QinThe Fourth Clinical School of Nanjing Medical University, Nanjing 210029, China.
Siwen LiuDepartment of Chemotherapy, Nanjing Medical University Affiliated Cancer Hospital Cancer Institute of Jiangsu Province, Nanjing 210009, China.
Jifeng FengDepartment of Chemotherapy, Nanjing Medical University Affiliated Cancer Hospital Cancer Institute of Jiangsu Province, Nanjing 210009, China.
Jiangsu Cancer Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study was to systemically analyze the mechanism of LXR ligand GW3965-induced sensitivity to EGFR-TKI in EGFR-TKI-resistant non-small cell lung cancer (NSCLC) cell lines.

methodsGefitinib-resistant PC9 cell line (EGFR exon 19 deletion) was treated with single and combined treatment with GW3965 and gefitinib. Cell viability, apoptosis and autophagy were detected using MTT, flow cytometric analysis and immunofluorescent analysis, respectively. Autophagy-related signaling pathways were detected using Western blot analysis.

resultsInhibited cell viability by single and combined treatment with gefitinib and GW3965 were observed. Combined treatment with gefitinib and GW3965 increased LC3 II/I ratio and Beclin 1 expression. Synergistic effect of gefitinib and GW3965 on apoptosis and autophagosome accumulation as well as on the inhibition of Akt/mTOR signaling and activation of AMP-activated protein kinase (AMPK) was observed in gefitinib-resistant PC9 cells. AMPK expression showed similar profile with apoptosis and autophagy of PC9 cells.

conclusionsWe confirmed that GW3965 and gefitinib showed synergistic effect on Akt/mTOR inhibition, apoptosis and autophagy of lung cancer cells. Gefitinib sensitivity in PC9 cell line might be mediated by Akt/mTOR, AMPK and JNK signaling pathways.

Indexed as

Akt/mTORAutophagygefitinibGW3965non-small cell lung cancer (NSCLC)

Identifiers

PMID35116735
PMCPMC8797756
OpenAlexW4249164914

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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.