Evidence map›Paper›PMID 29901268›Full record

ArticleProteomics2018

Integrative Analysis of Proteome and Ubiquitylome Reveals Unique Features of Lysosomal and Endocytic Pathways in Gefitinib-Resistant Non-Small Cell Lung Cancer Cells.

Wang Li, Heyong Wang, Yan Yang, Tian Zhao, Zhixiong Zhang, Ye Tian, Zhaomie Shi, Xiaojun Peng, Fei Li, Yonghong Feng and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Proteomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. SMARCB1 regulates the hypoxic stress response in sickle cell trait.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Review
  8. Article
  9. FromCells · 2022
    Review
  10. Article
  11. The Analysis of the Ubiquitylomic Responses toJournal of inflammation research · 2022
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
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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

13 authors at 3 institutions in 2 countries.

Wang LiDepartment of Thoracic Surgery, Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, School of Life Science and Technology, Tongji University, Shanghai, 200433, P. R. China.
Heyong WangDepartment of Thoracic Surgery, Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, School of Life Science and Technology, Tongji University, Shanghai, 200433, P. R. China.
Yan YangDepartment of Thoracic Surgery, Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, School of Life Science and Technology, Tongji University, Shanghai, 200433, P. R. China.
Tian ZhaoDepartment of Thoracic Surgery, Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, School of Life Science and Technology, Tongji University, Shanghai, 200433, P. R. China.
Zhixiong ZhangDepartment of Thoracic Surgery, Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, School of Life Science and Technology, Tongji University, Shanghai, 200433, P. R. China.
Ye TianDepartment of Thoracic Surgery, Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, School of Life Science and Technology, Tongji University, Shanghai, 200433, P. R. China.
Zhaomie ShiJingjie PTM BioLab Co. Ltd., Hangzhou Economic and Technological Development Area, Hangzhou, 310018, P. R. China.
Xiaojun PengJingjie PTM BioLab Co. Ltd., Hangzhou Economic and Technological Development Area, Hangzhou, 310018, P. R. China.
Fei LiDepartment of Biology, New York University, New York, NY, 10003, USA.
Yonghong FengDepartment of Thoracic Surgery, Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, School of Life Science and Technology, Tongji University, Shanghai, 200433, P. R. China.
Lei ZhangDepartment of Thoracic Surgery, Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, School of Life Science and Technology, Tongji University, Shanghai, 200433, P. R. China.
Gening JiangDepartment of Thoracic Surgery, Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, School of Life Science and Technology, Tongji University, Shanghai, 200433, P. R. China.
Fan ZhangDepartment of Thoracic Surgery, Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, School of Life Science and Technology, Tongji University, Shanghai, 200433, P. R. China.ORCID 0000-0003-4068-3726
Tongji University · CNNew England Biolabs (China) · CNNew York University · US

Funding

Molecular Basis of Centromere Specification and InheritanceR01GM106037 · NIGMS · NEW YORK UNIVERSITY · PI LI, FEI · 2014 to 2018
$1.5M
NIGMS NIH HHS R01 GM106037
6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) patients carrying EGFR activating mutations treated with gefitinib, a tyrosine kinase inhibitor, will develop drug resistance. Ubiquitylation is one of major posttranslational modifications of proteins affecting the stability or function of proteins. However, the role of protein ubiquitylation in gefitinib resistance is poorly understood. To systematically identify the global change in protein expression and ubiquitylation during gefitinib resistance, a quantitative global proteome and ubiquitylome study in a pair of gefitinib-resistant and sensitive NSCLC cells is carried out. Altogether, changes in expression of 3773 proteins are quantified, and changes in ubiquitylation of 2893 lysine sites in 1415 proteins are measured in both cells. Interestingly, lysosomal and endocytic pathways, which are involved in autophagy regulation, are enriched with upregulated proteins or ubiquitylated proteins in gefitinib-resistant cells. In addition, HMGA2 overexpression or ALOX5 knockdown suppresses gefitinib resistance in NSCLC cells by inhibiting autophagy. Overall, these results reveal the previously unknown global ubiquitylome and proteomic features associated with gefitinib resistance, uncover the opposing roles of HMGA2 or ALOX5 in regulating gefitinib resistance and autophagy, and will help to identify new therapeutic targets in overcoming gefitinib resistance.

Indexed as

Drug Resistance, NeoplasmArachidonate 5-LipoxygenaseAutophagyCarcinoma, Non-Small-Cell LungEndosomesGefitinibGene OntologyHMGA2 ProteinHumansLung NeoplasmsLysosomesMass SpectrometryProtein Kinase InhibitorsProtein Processing, Post-TranslationalProteomeTumor Cells, CulturedALOX5 protein, humanArachidonate 5-LipoxygenaseGefitinibHMGA2 ProteinHMGA2 protein, humanProtein Kinase InhibitorsProteomeUbiquitingefitinib resistancenon-small cell lung cancerproteomeubiquitylome

Identifiers

PMID29901268
PMCPMC6099292
OpenAlexW2808346532

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.