Evidence map›Paper›PMID 10229197›Full record

ArticleOncogene1999

Oxamflatin is a novel antitumor compound that inhibits mammalian histone deacetylase.

Y B Kim, K H Lee, K Sugita, M Yoshida, S Horinouchi

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.9field-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

47 citing papers in PubMed, 235 citations in OpenAlex.

  1. Article
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  10. Chemical and structural biology of protein lysine deacetylases.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2017
    Review
  11. Article
  12. Review
  13. Bioactive heterocycles containing endocyclic N-hydroxy groups.European journal of medicinal chemistry · 2015
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
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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 1 country.

Y B KimDepartment of Biotechnology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Japan.
K H Lee
K Sugita
M Yoshida
S Horinouchi
The University of Tokyo · JPShionogi (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxamflatin [(2E)-5-[3-[(phenylsufonyl) aminol phenyl]-pent-2-en-4-ynohydroxamic acid] induces transcriptional activation of junD and morphological reversion in various NIH3T3-derived transformed cell lines. We found that oxamflatin showed in vitro antiproliferative activity against various mouse and human tumor cell lines with drastic changes in the cell morphology and in vivo antitumor activity against B16 melanoma. Oxamflatin caused an elongated cell shape with filamentous protrusions as well as arrest of the cell cycle at the G1 phase in HeLa cells. These phenotypic changes of HeLa cells were apparently similar to those by trichostatin A (TSA), a specific inhibitor of histone deacetylase (HDAC). The effect of oxamflatin on the transcriptional activity of the cytomegalovirus (CMV) promoter was examined and compared with known HDAC inhibitors, TSA, sodium n-butyrate, and FR901228. Oxamflatin as well as all these inhibitors greatly enhanced the transcriptional activity of the CMV promoter in a dose-dependent manner. Oxamflatin, like TSA, inhibited intracellular HDAC activity, as a result of which marked amounts of acetylated histone species accumulated. Finally, effects on expression of several endogenous genes involved in cell morphology and cell cycle control in HeLa cells were analysed. Expression of gelsolin, cyclin E and Cdk inhibitors including p21WAF1/Cip1 was highly augmented, while that of cyclin A and cyclin D1 was decreased by oxamflatin. These results suggest that changes in the expression pattern of the genes regulating cell morphology and the cell cycle due to histone hyperacetylation are responsible for the antitumor activity, the morphological change and the cell cycle arrest induced by oxamflatin.

Indexed as

CDC2-CDC28 KinasesHistone Deacetylase InhibitorsProto-Oncogene ProteinsAnimalsAntineoplastic AgentsCell DivisionCyclin ACyclin D1Cyclin-Dependent Kinase 2Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent KinasesCyclinsCytomegalovirusDrug Screening Assays, AntitumorEnzyme InhibitorsAntineoplastic AgentsCDC2-CDC28 KinasesCDK2 protein, humanCdk2 protein, mouseCDK4 protein, humanCdk4 protein, mouseCDKN1A protein, humanCdkn1a protein, mouseCyclin ACyclin D1Cyclin-Dependent Kinase 2Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent KinasesCyclinsEnzyme InhibitorsGelsolinHistone Deacetylase InhibitorsHydroxamic AcidsoxamflatinProtein Serine-Threonine KinasesProto-Oncogene Proteinstrichostatin A

Identifiers

PMID10229197
OpenAlexW1998475911

What OpenQuestion holds

Textmetadata
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.