Evidence map›Paper›PMID 33943009›Full record

ArticleThoracic cancer2021

Targeting the EMT transcription factor Snail overcomes resistance to osimertinib in EGFR-mutant non-small cell lung cancer.

Qiong Qin, Xiaoqing Li, Xingmei Liang, Lili Zeng, Jing Wang, Linlin Sun, Diansheng Zhong

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  6. Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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  19. SOS2 regulates the threshold of mutantbioRxiv : the preprint server for biology · 2023
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Qiong QinDepartment of Oncology, Tianjin Medical University General Hospital, Tianjin, China.ORCID 0000-0002-0222-0715
Xiaoqing LiPhase I clinical trail Department, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Xingmei LiangDepartment of Oncology, Tianjin Medical University General Hospital, Tianjin, China.
Lili ZengDepartment of Oncology, Tianjin Medical University General Hospital, Tianjin, China.
Jing WangTianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin, China.
Linlin SunTianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin, China.
Diansheng ZhongDepartment of Oncology, Tianjin Medical University General Hospital, Tianjin, China.ORCID 0000-0001-6483-8134
Tianjin Medical University General Hospital · CNTianjin Medical University Cancer Institute and Hospital · CN

Funding

National Natural Science Foundation of China 31301160National Natural Science Foundation of China 81572268National Natural Science Foundation of China 81972186Natural Science Foundation of Tianjin 16JCYBJC24400Natural Science Foundation of Tianjin 17JCYBJC25500
6 · The paper itself

Abstract

backgroundThe resistance mechanism of the third generation of epidermal growth factor (EGFR) tyrosine kinase inhibitor (TKI) osimertinib is complex. Epithelial mesenchymal transition (EMT) is a common mechanism of EGFR-TKI acquired resistance. Snail is an important transcription factor related to EMT. Whether targeting Snail can reverse the resistance of osimertinib by downregulating Snail is unknown.

methodsThe presence of EMT in H1975/OR (osimertinib resistance) cells was confirmed by transwell assay. To explore the EMT role in resistance, the expression levels of EMT markers were detected in both parental cells H1975 and resistant cells H1975OR. We used RNA interference technology to knockdown the key regulator Snail in resistant cells. After the interference efficiency was confirmed, changes in EMT-related molecules of Snail were explicitly downregulated, and changes in sensitivity and migration and invasion ability were also examined. We used CDK4/6 inhibitor to test the ability of reversing drug resistance by downregulating Snail.

resultsCompared with the H1975 cell line, the H1975/OR resistant cell line showed increased invasiveness, upregulated expression of vimentin and downregulation of E-cadherin. EMT occurred in the H1975/OR resistant cell line. The expression of Snail was upregulated in the osimertinib-resistant cell line H1975/OR. Knockdown of Snail increased the sensitivity of H1975/OR cells to osimertinib. CDK4/6 inhibitor palbociclib could downregulate the expression of Snail. CDK 4/6 inhibitor palbociclib combined with osimertinib could reverse the resistance of osimertinib in H1975/OR.

conclusionsSnail plays an important role in the third generation of EGFR-TKI osimertinib resistance, which may be reversed by downregulating Snail.

Indexed as

AcrylamidesAniline CompoundsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionErbB ReceptorsHumansIndolesLung NeoplasmsPyrimidinesSnail Family Transcription FactorsAcrylamidesAniline CompoundsEGFR protein, humanErbB ReceptorsIndolesosimertinibPyrimidinesSnail Family Transcription Factorsacquired resistanceCDK4/6 inhibitorepithelial-mesenchymal transition (EMT)Snailtyrosine kinase inhibitor (TKI)

Identifiers

PMID33943009
PMCPMC8169301
OpenAlexW3157490474

What Socratic 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 Socratic graph.