Evidence map›Paper›PMID 38942760›Full record

ArticleCell death & disease2024

Promotion of stem cell-like phenotype of lung adenocarcinoma by FAM83A via stabilization of ErbB2.

Ye Yuan, Liang Hao, Jing-Shan Huang, Fu-Ying Zhao, Ying-Hua Ju, Jia-Mei Wang, Ting Zhang, Bai-Qiang Li, Zhan-Wu Yu

Erratum issuedAbstract read
In one paragraph

Article in Cell death & disease, 2024. 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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Human mutation · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Ye Yuan *Central Laboratory, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, 110042, China.
Liang Hao *Department of Biochemistry & Molecular Biology, China Medical University, Shenyang, 110026, China.
Jing-Shan Huang *Department of Biochemistry & Molecular Biology, China Medical University, Shenyang, 110026, China.ORCID http://orcid.org/0009-0006-1977-303X
Fu-Ying ZhaoDepartment of Biochemistry & Molecular Biology, China Medical University, Shenyang, 110026, China.
Ying-Hua JuDepartment of Biochemistry & Molecular Biology, China Medical University, Shenyang, 110026, China.
Jia-Mei WangDepartment of Laboratory Medicine, the 1st affiliated hospital, China Medical University, Shenyang, 110001, China.
Ting ZhangDepartment of Biochemistry & Molecular Biology, China Medical University, Shenyang, 110026, China.
Bai-Qiang LiDepartment of Biochemistry & Molecular Biology, China Medical University, Shenyang, 110026, China.
Zhan-Wu YuDepartment of Thoracic Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology, Shenyang, 110042, China. yuzhanwu1974@163.com.ORCID http://orcid.org/0000-0003-1076-2140

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82103693
6 · The paper itself

Abstract

Lung cancer stands as the leading cause of mortality among all types of tumors, with over 40% of cases being lung adenocarcinoma (LUAD). Family with sequence similarity 83 member A (FAM83A) emerges as a notable focus due to its frequent overexpression in LUAD. Despite this, the precise role of FAM83A remains elusive. This study addresses this gap by unveiling the crucial involvement of FAM83A in maintaining the cancer stem cell-like (CSC-like) phenotype of LUAD. Through a global proteomics analysis, the study identifies human epidermal growth factor receptor 2 (HER2 or ErbB2) as a crucial target of FAM83A. Mechanistically, FAM83A facilitated ErbB2 expression at the posttranslational modification level via the E3 ubiquitin ligase STUB1 (STIP1-homologous U-Box containing protein 1). More importantly, the interaction between FAM83A and ErbB2 at Arg241 promotes calcineurin (CALN)-mediated dephosphorylation of ErbB2, followed by inhibition of STUB1-mediated ubiquitin-proteasomal ErbB2 degradation. The maintenance of the CSC-like phenotype by FAM83A, achieved through the posttranslational regulation of ErbB2, offers valuable insights for identifying potential therapeutic targets for LUAD.

Indexed as

Adenocarcinoma of LungErb-b2 Receptor Tyrosine KinasesLung NeoplasmsNeoplasm ProteinsNeoplastic Stem CellsPhenotypeAnimalsCell Line, TumorFemaleHumansMiceUbiquitin-Protein LigasesERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesFAM83A protein, humanNeoplasm ProteinsUbiquitin-Protein Ligases

Identifiers

PMID38942760
PMCPMC11213963

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