Evidence map›Paper›PMID 29549343›Full record

ArticleCell death & disease2018

NF-κB-driven improvement of EHD1 contributes to erlotinib resistance in EGFR-mutant lung cancers.

Xiaoyuan Wang, Hang Yin, Hongxia Zhang, Jing Hu, Hailing Lu, Chunhong Li, Mengru Cao, Shi Yan, Li Cai

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
6.8field-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

22 citing papers in PubMed, 49 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

9 authors at 2 institutions in 1 country.

Xiaoyuan WangThe Department of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Hang YinThe Department of Radiotherapy Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Hongxia ZhangThe Department of MRI, Harbin Medical University Cancer Hospital, Harbin, China.
Jing HuThe Department of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Hailing LuThe Department of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Chunhong LiThe Department of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Mengru CaoThe Department of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Shi YanThe Department of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Li CaiThe Department of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China. caiwenxin76@163.com.
Harbin Medical University · CNThird Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acquired resistance to epidermal growth factor receptor-tyrosine-kinase inhibitors (EGFR-TKIs), such as gefitinib and erlotinib, is a critical obstacle in the treatment of EGFR mutant-positive non-small cell lung cancer (NSCLC). EHD1, a protein of the C-terminal Eps15 homology domain-containing (EHD) family, plays a role in regulating endocytic recycling, but the mechanistic details involved in EGFR-TKI resistance and cancer stemness remain largely unclear. Here, we found that a lower EHD1 expression improved both EGFR-TKIs sensitivity, which is consistent with a lower CD133 expression, and progression-free survival in NSCLC patients. The overexpression of EHD1 markedly increased erlotinib resistance and lung cancer cell stemness in vitro and in vivo. Moreover, we demonstrated that miR-590 targeted the 3'-UTR of EHD1 and was regulated by NK-κB, resulting in downregulated EHD1 expression, increased erlotinib sensitivity and repressed NSCLC cancer stem-like properties in vitro and in vivo. We found that EHD1 was an important factor in EGFR-TKI resistance and the cancer stem-like cell phenotype of lung cancer, and these results suggest that targeting the NF-κB/miR-590/EHD1 pathway has potential therapeutic promise in EGFR-mutant NSCLC patients with acquired EGFR-TKI resistance.

Indexed as

3' Untranslated RegionsAnimalsAntagomirsCarcinoma, Non-Small-Cell LungCell Line, TumorDown-RegulationDrug Resistance, NeoplasmErbB ReceptorsErlotinib HydrochlorideHumansLung NeoplasmsMiceMice, NudeMicroRNAsNF-kappa BProgression-Free Survival3' Untranslated RegionsAntagomirsEGFR protein, humanEHD1 protein, humanErbB ReceptorsErlotinib HydrochlorideMicroRNAsMIRN590 microRNA, humanNF-kappa BProtein Kinase InhibitorsRNA, Small InterferingVesicular Transport Proteins

Identifiers

PMID29549343
PMCPMC5856828
OpenAlexW2793586303

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.