Evidence map›Paper›PMID 32784836›Full record

ArticleCells2020

S-Adenosylmethionine Treatment of Colorectal Cancer Cell Lines Alters DNA Methylation, DNA Repair and Tumor Progression-Related Gene Expression.

Sára Zsigrai, Alexandra Kalmár, Zsófia B Nagy, Barbara K Barták, Gábor Valcz, Krisztina A Szigeti, Orsolya Galamb, Titanilla Dankó, Anna Sebestyén, Gábor Barna and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

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  12. Camptothecin Encapsulated in β-Cyclodextrin-EDTA-FeNanomaterials (Basel, Switzerland) · 2021
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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

18 authors at 2 institutions in 1 country.

Sára ZsigraiDepartment of Internal Medicine and Oncology, Semmelweis University, 1083 Budapest, Hungary.
Alexandra KalmárDepartment of Internal Medicine and Oncology, Semmelweis University, 1083 Budapest, Hungary.
Zsófia B NagyDepartment of Internal Medicine and Oncology, Semmelweis University, 1083 Budapest, Hungary.
Barbara K BartákDepartment of Internal Medicine and Oncology, Semmelweis University, 1083 Budapest, Hungary.
Gábor ValczDepartment of Internal Medicine and Oncology, Semmelweis University, 1083 Budapest, Hungary.
Krisztina A SzigetiDepartment of Internal Medicine and Oncology, Semmelweis University, 1083 Budapest, Hungary.
Orsolya GalambDepartment of Internal Medicine and Oncology, Semmelweis University, 1083 Budapest, Hungary.
Titanilla Dankó1st Department of Pathology and Experimental Cancer Research, Semmelweis University, 1085 Budapest, Hungary.
Anna Sebestyén1st Department of Pathology and Experimental Cancer Research, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0001-8814-4794
Gábor Barna1st Department of Pathology and Experimental Cancer Research, Semmelweis University, 1085 Budapest, Hungary.
Vanessza Szabó1st Department of Pathology and Experimental Cancer Research, Semmelweis University, 1085 Budapest, Hungary.
Orsolya PipekDepartment of Physics of Complex Systems, ELTE Eötvös Loránd University, 1117 Budapest, Hungary.
Anna Medgyes-HorváthDepartment of Physics of Complex Systems, ELTE Eötvös Loránd University, 1117 Budapest, Hungary.ORCID 0000-0003-4435-5797
István CsabaiDepartment of Physics of Complex Systems, ELTE Eötvös Loránd University, 1117 Budapest, Hungary.
Zsolt TulassayMTA-SE Molecular Medicine Research Group, Hungarian Academy of Sciences, 1051 Budapest, Hungary.
Péter IgazDepartment of Internal Medicine and Oncology, Semmelweis University, 1083 Budapest, Hungary.ORCID 0000-0003-2192-554X
István TakácsDepartment of Internal Medicine and Oncology, Semmelweis University, 1083 Budapest, Hungary.
Béla MolnárDepartment of Internal Medicine and Oncology, Semmelweis University, 1083 Budapest, Hungary.
Semmelweis University · HUEötvös Loránd University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Global DNA hypomethylation is a characteristic feature of colorectal carcinoma (CRC). The tumor inhibitory effect of S-adenosylmethionine (SAM) methyl donor has been described in certain cancers including CRC. However, the molecular impact of SAM treatment on CRC cell lines with distinct genetic features has not been evaluated comprehensively. HT-29 and SW480 cells were treated with 0.5 and 1 mmol/L SAM for 48 h followed by cell proliferation measurements, whole-genome transcriptome and methylome analyses, DNA stability assessments and exome sequencing. SAM reduced cell number and increased senescence by causing S phase arrest, besides, multiple EMT-related genes (e.g.,

Indexed as

Antineoplastic AgentsCarcinomaColorectal NeoplasmsDNA MethylationDNA RepairGene Expression Regulation, NeoplasticHT29 CellsHumansS-AdenosylmethionineAntineoplastic AgentsS-Adenosylmethioninecancer therapycolorectal cancerDNA methylationEMTepigeneticsgenomic stabilityS-adenosylmethionine

Identifiers

PMID32784836
PMCPMC7464653
OpenAlexW3047951122

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.