Evidence map›Paper›PMID 22037302›Full record

ReviewBiochimica et biophysica acta2012

The 26S proteasome complex: an attractive target for cancer therapy.

Sarah Frankland-Searby, Sukesh R Bhaumik

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

97 citing papers in PubMed, 176 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. The Role of the Ubiquitin System in Eye Diseases.Life (Basel, Switzerland) · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Facilitates Chromatin Transcription in Breast and Other Cancers.Advances in experimental medicine and biology · 2024
    Review
  15. UPS writes a new saga of SAGA.Biochimica et biophysica acta. Gene regulatory mechanisms · 2023
    Review
  16. Inhibitors Targeting the F-BOX Proteins.Cell biochemistry and biophysics · 2023
    Review
  17. Review
  18. Article
  19. Article
  20. Article

37 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Sarah Frankland-SearbyDepartment of Biochemistry and Molecular Biology, Southern Illinois University School of Medicine, Carbondale, IL 62901, USA.
Sukesh R Bhaumik
Southern Illinois University School of Medicine · US

Funding

Ubiquitin-proteasome system regulation of a transcriptional co-activator, SAGA, and associated functionsR15GM088798 · NIGMS · SOUTHERN ILLINOIS UNIVERSITY CARBONDALE · PI BHAUMIK, SUKESH R. · 2009 to 2018
$997k
NIGMS NIH HHS 1R15GM088798-01NIGMS NIH HHS R15 GM088798PHS HHS 10GRNT4300059
6 · The paper itself

Abstract

The 26S proteasome complex engages in an ATP-dependent proteolytic degradation of a variety of oncoproteins, transcription factors, cell cycle specific cyclins, cyclin-dependent kinase inhibitors, ornithine decarboxylase, and other key regulatory cellular proteins. Thus, the proteasome regulates either directly or indirectly many important cellular processes. Altered regulation of these cellular events is linked to the development of cancer. Therefore, the proteasome has become an attractive target for the treatment of numerous cancers. Several proteasome inhibitors that target the proteolytic active sites of the 26S proteasome complex have been developed and tested for anti-tumor activities. These proteasome inhibitors have displayed impressive anti-tumor functions by inducing apoptosis in different tumor types. Further, the proteasome inhibitors have been shown to induce cell cycle arrest, and inhibit angiogenesis, cell-cell adhesion, cell migration, immune and inflammatory responses, and DNA repair response. A number of proteasome inhibitors are now in clinical trials to treat multiple myeloma and solid tumors. Many other proteasome inhibitors with different efficiencies are being developed and tested for anti-tumor activities. Several proteasome inhibitors currently in clinical trials have shown significantly improved anti-tumor activities when combined with other drugs such as histone deacetylase (HDAC) inhibitors, Akt (protein kinase B) inhibitors, DNA damaging agents, Hsp90 (heat shock protein 90) inhibitors, and lenalidomide. The proteasome inhibitor bortezomib is now in the clinic to treat multiple myeloma and mantle cell lymphoma. Here, we discuss the 26S proteasome complex in carcinogenesis and different proteasome inhibitors with their potential therapeutic applications in treatment of numerous cancers.

Indexed as

Proteasome InhibitorsAntineoplastic AgentsCell Transformation, NeoplasticClinical Trials as TopicHumansMolecular Targeted TherapyNeoplasmsProtease InhibitorsProteasome Endopeptidase ComplexAntineoplastic AgentsATP dependent 26S proteaseProtease InhibitorsProteasome Endopeptidase ComplexProteasome Inhibitors

Identifiers

PMID22037302
PMCPMC3242858
OpenAlexW2013237763

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.