Evidence map›Paper›PMID 26804424›Full record

ReviewSeminars in cancer biology2016

F-BOX proteins in cancer cachexia and muscle wasting: Emerging regulators and therapeutic opportunities.

Ammar Sukari, Irfana Muqbil, Ramzi M Mohammad, Philip A Philip, Asfar S Azmi

Abstract readReview
In one paragraph

Review in Seminars in cancer biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

34 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Long-chain Polyunsaturated Fatty Acids MitigatebioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Frontiers in nutrition · 2025
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Frontiers in pharmacology · 2024
    Article
  17. Development of a peptide drug restoring AMPK and adipose tissue functionality in cancer cachexia.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  18. Review
  19. Article
  20. Article
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 2 institutions in 2 countries.

Ammar SukariDepartment of Oncology, Wayne State University School of Medicine, Karmanos Cancer Institute, Detroit, MI 48201, USA.
Irfana MuqbilDepartment of Oncology, Wayne State University School of Medicine, Karmanos Cancer Institute, Detroit, MI 48201, USA.
Ramzi M MohammadDepartment of Oncology, Wayne State University School of Medicine, Karmanos Cancer Institute, Detroit, MI 48201, USA; iTRI Hamad Medical Corporation, Doha, Qatar.
Philip A PhilipDepartment of Oncology, Wayne State University School of Medicine, Karmanos Cancer Institute, Detroit, MI 48201, USA.
Asfar S AzmiDepartment of Oncology, Wayne State University School of Medicine, Karmanos Cancer Institute, Detroit, MI 48201, USA. Electronic address: azmia@karmanos.org.
The Barbara Ann Karmanos Cancer Institute · USWayne State University · US

Funding

Targeting PAK4 for Overcoming Drug Resistance in Pancreatic CancerR21CA188818 · NCI · WAYNE STATE UNIVERSITY · PI AZMI, ASFAR S, MOHAMMAD, RAMZI M. · 2015 to 2016
$366k
NCI NIH HHS 1R21CA188818-01A1NCI NIH HHS R21 CA188818
6 · The paper itself

Abstract

Cancer cachexia is a debilitating metabolic syndrome accounting for fatigue, an impairment of normal activities, loss of muscle mass associated with body weight loss eventually leading to death in majority of patients with advanced disease. Cachexia patients undergoing skeletal muscle atrophy show consistent activation of the SCF ubiquitin ligase (F-BOX) family member Atrogin-1 (also known as MAFBx/FBXO32) alongside the activation of the muscle ring finger protein1 (MuRF1). Other lesser known F-BOX family members are also emerging as key players supporting muscle wasting pathways. Recent work highlights a spectrum of different cancer signaling mechanisms impacting F-BOX family members that feed forward muscle atrophy related genes during cachexia. These novel players provide unique opportunities to block cachexia induced skeletal muscle atrophy by therapeutically targeting the SCF protein ligases. Conversely, strategies that induce the production of proteins may be helpful to counter the effects of these F-BOX proteins. Through this review, we bring forward some novel targets that promote atrogin-1 signaling in cachexia and muscle wasting and highlight newer therapeutic opportunities that can help in the better management of patients with this devastating and fatal disorder.

Indexed as

AnimalsAntineoplastic AgentsBiological ProductsCachexiaF-Box ProteinsGene Expression Regulation, LeukemicHumansIntracellular SpaceMolecular Targeted TherapyMultiprotein ComplexesMuscular AtrophyNeoplasmsProtein BindingProtein TransportSignal TransductionSKP Cullin F-Box Protein LigasesAntineoplastic AgentsBiological ProductsF-Box ProteinsMultiprotein ComplexesSKP Cullin F-Box Protein LigasesAtrogin-1Cancer cachexiaCRM1F-BOXMuscle wasting

Identifiers

PMID26804424
PMCPMC4761518
OpenAlexW2255596096

What OpenQuestion holds

Textmetadata
LicenceTDM
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.