Evidence map›Paper›PMID 29855336›Full record

ArticleJournal of hematology & oncology2018

The role of HGF-MET pathway and CCDC66 cirRNA expression in EGFR resistance and epithelial-to-mesenchymal transition of lung adenocarcinoma cells.

Nithila A Joseph, Shiow-Her Chiou, Zoe Lung, Cheng-Lin Yang, Tze-Yi Lin, Hui-Wen Chang, H Sunny Sun, Sachin Kumar Gupta, Laising Yen, Shulhn-Der Wang and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of hematology & oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 73 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

11 authors at 5 institutions in 2 countries.

Nithila A JosephGraduate Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan.
Shiow-Her ChiouGraduate Institute of Microbiology and Public Health, National Chung Hsing University, Taichung, Taiwan. shchiou@dragon.nchu.edu.tw.
Zoe LungDepartment of Molecular and Cell Biology, University of California, Berkeley, CA, USA.
Cheng-Lin YangGraduate Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan.
Tze-Yi LinDepartment of Pathology, China Medical University Hospital, Taichung, Taiwan.
Hui-Wen ChangDepartment of Pathology, China Medical University Hospital, Taichung, Taiwan.
H Sunny SunInstitute of Molecular Medicine, National Chung Kung University, Tainan, Taiwan. hssun@mail.ncku.edu.tw.
Sachin Kumar GuptaDepartment of Pathology and Immunology, Baylor College of Medicine, Houston, TX, USA.
Laising YenDepartment of Pathology and Immunology, Baylor College of Medicine, Houston, TX, USA.
Shulhn-Der WangSchool of Post-Baccalaureate Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan.
Kuan-Chih ChowGraduate Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan. kcchow668@gmail.com.ORCID 0000-0002-0611-0337
National Chung Hsing University · TWChina Medical University · TWBaylor College of Medicine · USNational Cheng Kung University · TWUniversity of California, Berkeley · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpithelial-to-mesenchymal transition (EMT) has, in recent years, emerged as an important tumor cell behavior associated with high metastatic potential and drug resistance. Interestingly, protein SUMOylation and hepatocyte growth factor could respectively reduce the effect of small molecule inhibitors on tyrosine kinase activity of mutated epidermal growth factor receptor of lung adenocarcinomas (LADC). The actual mechanism is yet to be resolved.

methodsImmunohistochemistry was used to stain proteins in LADC specimens. Protein expression was confirmed by Western blotting. In vitro, expression of proteins was determined by Western blotting and immunocytochemistry. Levels of circular RNA were determined by reverse transcription-polymerase chain reaction.

resultsSAE2 and cirRNA CCDC66 were highly expressed in LADC. Expression of SAE2 was mainly regulated by EGFR; however, expression of cirRNA CCDC66 was positively regulated by FAK and c-Met but negatively modulated by nAchR7α. EGFR-resistant H1975 also highly expressed cirRNA CCDC66. Immediate response of hypoxia increased phosphorylated c-Met, SAE2, and epithelial-to-mesenchymal transition. Either activation of FAK or silencing of nAchR7α increased cirRNA CCDC66.

conclusionsHGF/c-Met regulates expression of SAE2 and cirRNA CCDC66 to increase EMT and drug resistance of LADC cells. Multimodality drugs concurrently aiming at these targets would probably provide more benefits for cancer patients.

Indexed as

AdenocarcinomaCell-Free Nucleic AcidsCell LineDrug ResistanceEpithelial-Mesenchymal TransitionErbB ReceptorsEye ProteinsGene ExpressionHepatocyte Growth FactorHumansLung NeoplasmsMetabolic Networks and PathwaysProto-Oncogene Proteins c-metUbiquitin-Activating EnzymesCCDC66 protein, humanCell-Free Nucleic AcidsEGFR protein, humanErbB ReceptorsEye ProteinsHepatocyte Growth FactorHGF protein, humanMET protein, humanProto-Oncogene Proteins c-metUBA2 protein, humanUbiquitin-Activating EnzymesCCDC66cirRNAc-METEGFREMTHGFSAE2SUMOylation

Identifiers

PMID29855336
PMCPMC5984410
OpenAlexW2807508331

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.