Evidence map›Paper›PMID 28459460›Full record

ArticleOncogene2017

MAGEA1 interacts with FBXW7 and regulates ubiquitin ligase-mediated turnover of NICD1 in breast and ovarian cancer cells.

J Zhao, Y Wang, C Mu, Y Xu, J Sang

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. F-box in breast cancer: mechanism of action and therapeutic potential.American journal of translational research · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. FBXW7 in breast cancer: mechanism of action and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2023
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. 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

5 authors at 1 institution in 2 countries.

J ZhaoKey Laboratory of Cell Proliferation and Regulation, College of Life Sciences, Beijing Normal University, Beijing, China.
Y WangKey Laboratory of Cell Proliferation and Regulation, College of Life Sciences, Beijing Normal University, Beijing, China.
C MuKey Laboratory of Cell Proliferation and Regulation, College of Life Sciences, Beijing Normal University, Beijing, China.
Y XuDepartment of Obstetrics and Gynecology, Indiana University School of Medicine, Indianapolis, IN, USA.
J SangKey Laboratory of Cell Proliferation and Regulation, College of Life Sciences, Beijing Normal University, Beijing, China.
Beijing Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma-associated antigen A1 (MAGEA1) is member of the MAGE gene family that is expressed in male germ line cells and placenta under normal physiological conditions. Although MAGEA1's expression levels have been evaluated as one of the cancer testis (CT) antigens for immunotherapy in melanoma and several other cancers, its functional role and signaling mechanisms are largely unknown. In this study, we examined the functional involvement and signaling mechanisms of MAGEA1 in breast and ovarian cancer cells. Inhibitory effects of MAGEA1 on cell proliferation and migration were observed using both gain-of- (MAGEA1 overexpression) and loss-of- (siRNA interference) function approaches in breast (MCF-7 and MDA-MB-231) and ovarian (SKOV3 and SKOV3ip) cancer cell lines. We revealed a novel interaction between MAGEA1 and the intracellular segment of NOTCH1 receptor (NICD1). MAGEA1 reduced NICD1's stability by promoting the ubiquitin modification of NICD1. MAGEA1 also interacted with FBXW7, subunit of E3 ubiquitin protein ligase complex SCF, and the latter was functionally involved in NICD1 ubiquitination and degradation. In addition, siRNA interference of FBXW7 reversed the inhibitory effect of MAGEA1 on migration and proliferation of MCF-7 and MDA-MB-231 cells. These newly discovered MAGEA1-NICD1 and MAGEA1-FBXW7 interactions have potential clinical implications in breast and ovarian cancer treatment.

Indexed as

Breast NeoplasmsCell Cycle ProteinsCell Line, TumorCell ProliferationF-Box ProteinsF-Box-WD Repeat-Containing Protein 7FemaleHumansMCF-7 CellsMelanoma-Specific AntigensOvarian NeoplasmsReceptor, Notch1Signal TransductionTransfectionUbiquitinationUbiquitin-Protein LigasesCell Cycle ProteinsF-Box ProteinsF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanMAGEA1 protein, humanMelanoma-Specific AntigensReceptor, Notch1Ubiquitin-Protein Ligases

Identifiers

PMID28459460
OpenAlexW2611644009

What OpenQuestion holds

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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.