Evidence map›Paper›PMID 23147569›Full record

ArticleToxicology and applied pharmacology2013

Vorinostat, an HDAC inhibitor attenuates epidermoid squamous cell carcinoma growth by dampening mTOR signaling pathway in a human xenograft murine model.

Deepali Kurundkar, Ritesh K Srivastava, Sandeep C Chaudhary, Mary E Ballestas, Levy Kopelovich, Craig A Elmets, Mohammad Athar

Abstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Molecular Mechanisms of Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Oh, the Mutations You'll Acquire! A Systematic Overview of Cutaneous Squamous Cell Carcinoma.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  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 1 country.

Deepali KurundkarDepartment of Dermatology and Skin Diseases Research Center, University of Alabama at Birmingham, 1530 3rd Avenue South, VH 509, Birmingham, AL 35294-0019, USA.
Ritesh K Srivastava
Sandeep C Chaudhary
Mary E Ballestas
Levy Kopelovich
Craig A Elmets
Mohammad Athar
University of Alabama at Birmingham · USChildren's of Alabama · USNational Cancer Institute · US

Funding

UAB Neuroscience Core CenterP30NS047466 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STANDAERT, DAVID G. · 2005 to 2019
$8.5M
Inhibiting Multiple Molecular Targets for Preventing Non-Melanoma Skin CancerR01CA138998 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ATHAR, MOHAMMAD · 2011 to 2015
$1.5M
Developing a murine model for arsenic-induced skin neoplasmR21ES017494 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ATHAR, MOHAMMAD · 2009 to 2010
$401k
NCI NIH HHS R01 CA138998NCI NIH HHS R01CA138998NIEHS NIH HHS R21 ES017494NINDS NIH HHS P30 NS047466NINDS NIH HHS P30NS047466
6 · The paper itself

Abstract

Histone deacetylase (HDAC) inhibitors are potent anticancer agents and show efficacy against various human neoplasms. Vorinostat is a potent HDAC inhibitor and has shown potential to inhibit growth of human xenograft tumors. However, its effect on the growth of skin neoplasm remains undefined. In this study, we show that vorinostat (2 μM) reduced expression of HDAC1, 2, 3, and 7 in epidermoid carcinoma A431 cells. Consistently, it increased acetylation of histone H3 and p53. Vorinostat (100mg/kg body weight, IP) treatment reduced human xenograft tumor growth in highly immunosuppressed nu/nu mice. Histologically, the vorinostat-treated tumor showed features of well-differentiation with large necrotic areas. Based on proliferating cell nuclear antigen (PCNA) staining and expression of cyclins D1, D2, E, and A, vorinostat seems to impair proliferation by down-regulating the expression of these proteins. However, it also induced apoptosis. The mechanism by which vorinostat blocks proliferation and makes tumor cells prone to apoptosis, involved inhibition of mTOR signaling which was accompanied by reduction in cell survival AKT and extracellular-signal regulated kinase (ERK) signaling pathways. Our data provide a novel mechanism-based therapeutic intervention for cutaneous squamous cell carcinoma (SCC). Vorinostat may be utilized to cure skin neoplasms in organ transplant recipient (OTR). These patients have high morbidity and surgical removal of these lesions which frequently develop in these patients, is difficult.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCarcinoma, Squamous CellCell ProliferationCell SurvivalCyclinsDose-Response Relationship, DrugDown-RegulationFemaleHistone Deacetylase InhibitorsHistone DeacetylasesHumansHydroxamic AcidsImmunocompromised HostMiceAntineoplastic AgentsCyclinsHistone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsProliferating Cell Nuclear AntigenTOR Serine-Threonine KinasesVorinostat

Identifiers

PMID23147569
PMCPMC3534787
OpenAlexW2093208648

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.