Evidence map›Paper›PMID 22447226›Full record

ArticleActa pharmacologica Sinica2012

FoxM1 mediated resistance to gefitinib in non-small-cell lung cancer cells.

Nuo Xu, Xin Zhang, Xun Wang, Hai-yan Ge, Xiao-ying Wang, David Garfield, Ping Yang, Yuan-lin Song, Chun-xue Bai

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  4. Review
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  6. Article
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  9. The multifaceted roles of FOXM1 in pulmonary disease.Cell communication and signaling : CCS · 2019
    Review
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  11. Article
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  16. Overexpressed transcription factor FOXM1 is a potential diagnostic and adverse prognostic factor in postoperational gastric cancer patients.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014
    Article
  17. Article
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  19. Prognostic significance of NSE mRNA in advanced NSCLC treated with gefitinib.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2013
    Article
  20. 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

9 authors at 6 institutions in 2 countries.

Nuo XuDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Xin Zhang
Xun Wang
Hai-yan Ge
Xiao-ying Wang
David Garfield
Ping Yang
Yuan-lin Song
Chun-xue Bai
Fudan University · CNFudan University Shanghai Cancer Center · CNMayo Clinic in Florida · USSun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimGefitinib is effective in only approximately 20% of patients with non-small-cell lung cancer (NSCLC), and the underlying mechanism remains unclear. FoxM1 is upregulated in NSCLC and associated with a poor prognosis in NSCLC patients. In this study, we examined the possible role of FoxM1 in gefitinib resistance and the related mechanisms.

methodsGefitinib resistant human lung adenocarcinoma cell line SPC-A-1 and gefitinib-sensitive human lung mucoepidermoid carcinoma cell line NCI-H292 were used. mRNA and protein expression of FoxM1 and other factors were tested with quantitative RT PCR and Western blot analysis. RNA interference was performed to suppress FoxM1 expression in SPC-A-1 cells, and lentiviral infection was used to overexpress FoxM1 in H292 cells. MTT assay and flow cytometry were used to examine the proliferation and apoptosis of the cells.

resultsTreatment of SPC-A-1 cells with gefitinib (1 and 10 μmol/L) upregulated the expression of FoxM1 in time- and concentration-dependent manners, while gefitinib (1 μmol/L) downregulated in H292 cells. In SPC-A-1 cells treated with gefitinib (1 μmol/L), the expression of several downstream targets of FoxM1, including survivin, cyclin B1, SKP2, PLK1, Aurora B kinase and CDC25B, were significantly upregulated. Overexpression of FoxM1 increased the resistance in H292 cells, while attenuated FoxM1 expression restored the sensitivity to gefitinib in SPC-A-1 cells by inhibiting proliferation and inducing apoptosis.

conclusionThe results suggest that FoxM1 plays an important role in the resistance of NSCLC cells to gefitinib in vitro. FoxM1 could be used as a therapeutic target to overcome the resistance to gefitinib.

Indexed as

Drug Resistance, NeoplasmAdenocarcinomaAdenocarcinoma of LungAntineoplastic AgentsApoptosisBlotting, WesternCarcinoma, MucoepidermoidCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationDose-Response Relationship, DrugFlow CytometryForkhead Box Protein M1Forkhead Transcription FactorsGefitinibGene Expression Regulation, NeoplasticAntineoplastic AgentsForkhead Box Protein M1Forkhead Transcription FactorsFOXM1 protein, humanGefitinibQuinazolinesRNA, Messenger

Identifiers

PMID22447226
PMCPMC4010351
OpenAlexW2079644390

What OpenQuestion holds

Textmetadata
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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.