Evidence map›Paper›PMID 26635117›Full record

ArticleScientific reports2015

Resveratrol overcomes gefitinib resistance by increasing the intracellular gefitinib concentration and triggering apoptosis, autophagy and senescence in PC9/G NSCLC cells.

Yinsong Zhu, Wenjuan He, Xiujuan Gao, Bin Li, Chenghan Mei, Rong Xu, Hui Chen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

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  18. Natural medicinal compounds target signal transduction pathways to overcome ABC drug efflux transporter-mediated multidrug resistance in cancer.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2023
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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

7 authors at 1 institution in 1 country.

Yinsong ZhuDepartment of Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Wenjuan HeDepartment of Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Xiujuan GaoDepartment of Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Bin LiDepartment of Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Chenghan MeiDepartment of Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Rong XuDepartment of Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Hui ChenDepartment of Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gefitinib (Gef) provides clinical benefits to non-small cell lung cancer (NSCLC) patients with activating EGFR mutations. However, acquired resistance (AR) is a major obstacle to effective Gef therapy. This study demonstrated that resveratrol (Res) could synergize with Gef to inhibit the proliferation of Gef-resistant NSCLC cells. The underlying mechanisms of synergism were investigated, and the results showed that cotreatment with Gef and Res could inhibit EGFR phosphorylation by increasing intracellular Gef accumulation through the impairment of Gef elimination from PC9/G cells. Consistently, CYP1A1 and ABCG2 expression were inhibited. Meanwhile, the cotreatment significantly induced cell apoptosis, autophagy, cell cycle arrest and senescence accompanied by increased expression of cleaved caspase-3, LC3B-II, p53 and p21. Further studies revealed that autophagy inhibition enhanced apoptosis and abrogated senescence while apoptosis inhibition had no notable effect on cell autophagy and senescence during cotreatment with Gef and Res. These results indicated that in addition to apoptosis, senescence promoted by autophagy contributes to the antiproliferation effect of combined Gef and Res on PC9/G cells. In conclusion, combined treatment with Gef and Res may represent a rational strategy to overcome AR in NSCLC cells.

Indexed as

Drug SynergismApoptosisATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2AutophagyCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCellular SenescenceCytochrome P-450 CYP1A1Drug Resistance, NeoplasmGefitinibGene Expression Regulation, NeoplasticHumansNeoplasm ProteinsQuinazolinesABCG2 protein, humanATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2CYP1A1 protein, humanCytochrome P-450 CYP1A1GefitinibNeoplasm ProteinsQuinazolinesResveratrolStilbenes

Identifiers

PMID26635117
PMCPMC4669414
OpenAlexW2280921381

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.