Evidence map›Paper›PMID 16826403›Full record

ArticleJournal of cancer research and clinical oncology2006

Mode of interaction between butyroyloxymethyl-diethyl phosphate (AN-7) and doxorubicin in MCF-7 and resistant MCF-7/Dx cell lines.

Dikla Engel, Abraham Nudelman, Inesa Levovich, Tal Gruss-Fischer, Michal Entin-Meer, Don R Phillips, Suzanne M Cutts, Ada Rephaeli

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 26 citations in OpenAlex.

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  6. Doxorubicin, DNA torsion, and chromatin dynamics.Biochimica et biophysica acta · 2014
    Review
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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

8 authors at 5 institutions in 3 countries.

Dikla EngelChemistry Department, Bar-Ilan University, Ramat Gan, 52900, Israel.
Abraham Nudelman
Inesa Levovich
Tal Gruss-Fischer
Michal Entin-Meer
Don R Phillips
Suzanne M Cutts
Ada Rephaeli
Bar-Ilan University · ILLa Trobe University · AURabin Medical Center · ILTel Aviv University · ILUniversity of California System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo investigate the anticancer activity and mode of action of butyroyloxymethyl-diethyl phosphate (AN-7), a prodrug of butyric acid and formaldehyde, as a single agent and in combination with doxorubicin in human carcinoma MCF-7 and the multidrug resistant MCF-7 Dx cell lines.

methodsThe anti-cancer activity of AN-7 as a single agent or in combination with doxorubicin was measured by the Hoechst cell viability and colony forming assays as well as by FACS analyses of cells stained with propidium iodide and annexin V-FITC. Modulations of protein expression and acetylation were measured by Western blot analyses. The number of doxorubicin-DNA adducts formed was evaluated using (14)C-labeled doxorubicin.

resultsThe AN-7 and homologous prodrugs exhibited similar growth inhibition effects against drug resistant and sensitive cells, and elicited their anticancer effect partially by inhibition of HDAC. The AN-7 transiently augmented histone acetylation and increase of p21 expression. Synergy between AN-7 and doxorubicin was demonstrated in the sensitive and the resistant cell lines by viability and colony formation assays and was further confirmed by FACS analysis showing an increase in cell mortality. The number of doxorubicin-DNA adducts in total genomic DNA isolated from cells treated with (14)C-labeled doxorubicin and AN-7 increased substantially compared to treatment with doxorubicin only. Treatment with AN-7 or doxorubicin increased p53 acetylation that was further potentiated by their combination.

conclusionThe AN-7 combined with doxorubicin overcame drug resistance; at least in part by the intracellularly releasable formaldehyde that augmented formation of doxorubicin-DNA adducts and butyric acid that induced histone and p53 acetylation. Since the use of doxorubicin is limited by toxicity, the combination could offer an effective treatment modality with lower toxicity for breast cancer.

Indexed as

AcetylationAntineoplastic Combined Chemotherapy ProtocolsBreast NeoplasmsButyratesCell Line, TumorCell SurvivalCyclin-Dependent Kinase Inhibitor p21DoxorubicinDrug Resistance, NeoplasmDrug SynergismFemaleHumansOrganophosphorus CompoundsProdrugsTumor Suppressor Protein p53ButyratesCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21diethoxyphosphoryloxymethyl butanoateDoxorubicinOrganophosphorus CompoundsProdrugsTumor Suppressor Protein p53

Identifiers

PMID16826403
PMCPMC12161022
OpenAlexW2088645604

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.