Evidence map›Paper›PMID 30714168›Full record

ArticleThe Journal of pathology2019

F-box protein FBXO16 functions as a tumor suppressor by attenuating nuclear β-catenin function.

Debasish Paul, Sehbanul Islam, Rajesh Kumar Manne, U S Dinesh, Sunil K Malonia, Biswanath Maity, Ramanamurthy Boppana, Srikanth Rapole, Praveen Kumar Shetty, Manas Kumar Santra

Open access · hybridAbstract read
In one paragraph

Article in The Journal of pathology, 2019. 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
2.1field-weighted citation impact, top 13% 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, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. GSK3β Regulates a Novel β-Catenin Degradation Pathway via the GID Complex in Wnt Signaling.Genes to cells : devoted to molecular & cellular mechanisms · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Inhibition of SCFCommunications biology · 2025
    Article
  8. F-box in breast cancer: mechanism of action and therapeutic potential.American journal of translational research · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

10 authors at 4 institutions in 2 countries.

Debasish PaulCancer Biology division, National Centre for Cell Science, Pune, India.
Sehbanul IslamCancer Biology division, National Centre for Cell Science, Pune, India.
Rajesh Kumar ManneCancer Biology division, National Centre for Cell Science, Pune, India.
U S DineshDepartment of Biochemistry/Central Research Laboratory, SDM College of Medical Sciences and Hospital, Dharwad, India.
Sunil K MaloniaDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA.
Biswanath MaityCentre of Biomedical Research, Lucknow, India.
Ramanamurthy BoppanaCancer Biology division, National Centre for Cell Science, Pune, India.
Srikanth RapoleCancer Biology division, National Centre for Cell Science, Pune, India.
Praveen Kumar ShettyDepartment of Biochemistry/Central Research Laboratory, SDM College of Medical Sciences and Hospital, Dharwad, India.
Manas Kumar SantraCancer Biology division, National Centre for Cell Science, Pune, India.ORCID 0000-0002-8899-4518
National Centre for Cell Science · INSDM College of Medical Science and Hospital · INCentre of Biomedical Research · INUniversity of Massachusetts Chan Medical School · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant activation of β-catenin has been implicated in a variety of human diseases, including cancer. In spite of significant progress, the regulation of active Wnt/β-catenin-signaling pathways is still poorly understood. In this study, we show that F-box protein 16 (FBXO16) is a putative tumor suppressor. It is a component of the SCF (SKP1-Cullin1-F-box protein) complex, which targets the nuclear β-catenin protein to facilitate proteasomal degradation through the 26S proteasome. FBXO16 interacts physically with the C-terminal domain of β-catenin and promotes its lysine 48-linked polyubiquitination. In addition, it inhibits epithelial-to-mesenchymal transition (EMT) by attenuating the level of β-catenin. Therefore, depletion of FBXO16 leads to increased levels of β-catenin, which then promotes cell invasion, tumor growth, and EMT of cancer cells. Furthermore, FBXO16 and β-catenin share an inverse correlation of cellular expression in clinical breast cancer patient samples. In summary, we propose that FBXO16 functions as a putative tumor suppressor by forming an SCF

Indexed as

beta CateninCell Line, TumorCell NucleusEpithelial-Mesenchymal TransitionF-Box ProteinsGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansNuclear ProteinsWnt Signaling Pathwaybeta CateninCTNNB1 protein, humanF-Box ProteinsFBXO16 protein, humanNuclear ProteinsFBXO16proteasomal degradationtumor suppressorWnt signalingβ-catenin

Identifiers

PMID30714168
PMCPMC6619347
OpenAlexW2913827684

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.