Evidence map›Paper›PMID 21508352›Full record

ArticleAnticancer research2011

Synergistic activity of histone deacetylase and proteasome inhibition against pancreatic and hepatocellular cancer cell lines.

J L Spratlin, T M Pitts, G N Kulikowski, M P Morelli, J J Tentler, N J Serkova, S G Eckhardt

Open access · greenAbstract read
In one paragraph

Article in Anticancer research, 2011. 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
1.9field-weighted citation impact, top 14% 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, 40 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Mechanism of Action for HDAC Inhibitors-Insights from Omics Approaches.International journal of molecular sciences · 2019
    Review
  8. Article
  9. Article
  10. Influence of media selection on NMR based metabolic profiling of human cell lines.Metabolomics : Official journal of the Metabolomic Society · 2018
    Article
  11. Review
  12. Review
  13. Article
  14. Metabolomics in pancreatic cancer biomarkers research.Medical oncology (Northwood, London, England) · 2016
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  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

7 authors at 3 institutions in 2 countries.

J L SpratlinCross Cancer Institute, University of Alberta, Edmonton, Alberta, Canada. jennifer.spratlin@albertahealthservices.ca
T M Pitts
G N Kulikowski
M P Morelli
J J Tentler
N J Serkova
S G Eckhardt
Livestrong Foundation · USUniversity of Alberta · CAUniversity of Colorado Denver · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
NCI NIH HHS P30 CA046934
6 · The paper itself

Abstract

aimTo determine the phenotypic effects of belinostat (bel) and bortezomib (bor) against pancreatic cancer (PC) and hepatocellular cancer (HCC) cell lines. MATERIALS AND

methodsAntiproliferative effects were assessed using a sulforhodamine B assay. Synergy was evaluated using the Chou and Talalay method. Apoptosis was measured by caspase-3/-7 activity and PARP cleavage. Downstream effector proteins were detected via immunoblotting. Quantitative nuclear magnetic resonance (NMR)-based metabolomics analysis was performed.

resultsThere were single-agent antiproliferative effects against PC and HCC cell lines; the combination of bel and bor (bel+bor) had a synergistic effect. There was up to a 45-fold induction of apoptosis over the control. Post-treatment cell death was associated with p21 up-regulation, more pronounced with treatment with bel+bor. Treatment with bel+bor enhanced hyperacetylation of histone H3 over single-agent bel. A metabolic signature was established for treatments with bor and bel+bor.

conclusionThe combination of bel+bor displayed significant antiproliferative activity against PC and HCC cell lines, with exhibiting synergistic antiproliferative and proapoptotic patterns even at suboptimal single-agent doses.

Indexed as

Proteasome InhibitorsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBoronic AcidsBortezomibCarcinoma, HepatocellularCaspase 3Cell Line, TumorDrug SynergismHistone Deacetylase InhibitorsHumansHydroxamic AcidsImmunoblottingLiver NeoplasmsMagnetic Resonance SpectroscopyMetabolomicsbelinostatBoronic AcidsBortezomibCaspase 3Histone Deacetylase InhibitorsHydroxamic AcidsProtease InhibitorsProteasome Endopeptidase ComplexProteasome InhibitorsPyrazinesSulfonamides

Identifiers

PMID21508352
PMCPMC3866806
OpenAlexW2163464088

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.