Evidence map›Paper›PMID 32552611›Full record

ArticleTherapeutic advances in respiratory disease

Combination therapy of gefitinib and miR-30a-5p may overcome acquired drug resistance through regulating the PI3K/AKT pathway in non-small cell lung cancer.

Fengfeng Wang, Fei Meng, Sze Chuen Cesar Wong, William C S Cho, Sijun Yang, Lawrence W C Chan

Open access · goldAbstract read
In one paragraph

Article in Therapeutic advances in respiratory disease. 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
3.5field-weighted citation impact, top 5% 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, 36 citations in OpenAlex.

  1. Review
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  9. MonitoringFrontiers in oncology · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. Functions of non-coding RNAs in regulating cancer drug targets.Acta biochimica et biophysica Sinica · 2022
    Review
  14. Review
  15. Article
  16. Cell Behavior of Non-Small Cell Lung Cancer Is at EGFR and MicroRNAs Hands.International journal of molecular sciences · 2021
    Review
  17. Review
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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

6 authors at 3 institutions in 2 countries.

Fengfeng WangDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong, P.R. China.
Fei MengDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong, P.R. China.
Sze Chuen Cesar WongDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong, P.R. China.
William C S ChoDepartment of Clinical Oncology, Queen Elizabeth Hospital, Hong Kong, P.R. China.
Sijun YangABSL-3 Laboratory at the Center for Animal Experiment and Institute of Animal Model for Human Disease, Wuhan University School of Medicine, Wuhan, P.R. China.
Lawrence W C ChanDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Y902, 9/F, Lee Shau Kee Building, Kowloon, Hong Kong, P.R. China.ORCID 0000-0001-6451-2273
Hong Kong Polytechnic University · HKQueen Elizabeth Hospital · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNon-small cell lung cancer (NSCLC) patients with an epidermal growth factor receptor (EGFR) mutation often initially respond to EGFR tyrosine kinase inhibitor (EGFR-TKI) treatment but may acquire drug resistance due to multiple factors. MicroRNAs are a class of small noncoding and endogenous RNA molecules that may play a role in overcoming the resistance. MATERIALS AND

methodsIn this study, we explored and validated, through

resultsDual inhibitors of EGFR and IGF1R significantly lowered the expression levels of phosphorylated protein kinase B (p-AKT) and phosphorylated mitogen-activated protein kinase (p-ERK) compared with the control group in all cell lines. With the ability to repress PI3K expression, miR-30a-5p mimics induced cell apoptosis, and inhibited cell invasion and migration in the treated H1650GR cell line.

conclusionGefitinib, combined with miR-30a-5p mimics, effectively suppressed the growth of H1650GR-induced tumor in xenografts. Hence, a combination therapy of gefitinib and miR-30a-5p may play a critical role in overcoming acquired resistance to EGFR-TKIs.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementFemaleGefitinibHumansLung NeoplasmsMice, Inbred BALB CMice, NudeMicroRNAsNeoplasm InvasivenessOligonucleotidesGefitinibMicroRNAsMIRN30b microRNA, humanOligonucleotidesPhosphatidylinositol 3-KinaseProtein Kinase InhibitorsProto-Oncogene Proteins c-aktcombination therapydrug resistanceepidermal growth factor receptorgefitinibmiR-30a-5pnon-small cell lung cancer

Identifiers

PMID32552611
PMCPMC7303773
OpenAlexW3036095792

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.