Evidence map›Paper›PMID 36077707›Full record

ArticleCancers2022

Enhanced Cytotoxicity on Cancer Cells by Combinational Treatment of PARP Inhibitor and 5-Azadeoxycytidine Accompanying Distinct Transcriptional Profiles.

Tomonori Araki, Kensuke Hamada, Aung Bhone Myat, Hideki Ogino, Kohei Hayashi, Miho Maeda, Ying Tong, Yasufumi Murakami, Kazuhiko Nakao, Mitsuko Masutani

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

10 authors at 3 institutions in 1 country.

Tomonori Araki *Department of Molecular and Genomic Biomedicine, Center for Bioinformatics and Molecular Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan.
Kensuke Hamada *Biochemistry Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Aung Bhone MyatDepartment of Molecular and Genomic Biomedicine, Center for Bioinformatics and Molecular Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan.
Hideki OginoBiochemistry Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Kohei HayashiDepartment of Molecular and Genomic Biomedicine, Center for Bioinformatics and Molecular Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan.ORCID 0000-0003-1780-4825
Miho MaedaBiochemistry Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Ying TongDepartment of Molecular and Genomic Biomedicine, Center for Bioinformatics and Molecular Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan.
Yasufumi MurakamiDepartment of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, Tokyo 162-8601, Japan.
Kazuhiko NakaoDepartment of Gastroenterology and Hepatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
Mitsuko MasutaniDepartment of Molecular and Genomic Biomedicine, Center for Bioinformatics and Molecular Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan.ORCID 0000-0003-2631-4334
Nagasaki University · JPTokyo University of Science · JPTokyo Medical and Dental University · JP

Funding

a Grant-in-Aid for the Second Term Comprehensive 10-Year Strategy for Cancer Control 2007-09a Grant-in-Aid from Almuni Association of Nagasaki University School of Medicine 2021-TAMinistry of Education, Culture, Sports, Science and Technology 2010-13Nagasaki University Priority Research Subject Project Based on Medium-term Goals and Plans 2017-HI
6 · The paper itself

Abstract

Poly(ADP-ribose) polymerase (PARP) is involved in DNA repair and chromatin regulation. 5-Aza-2'-deoxycytidine (5-aza-dC) inhibits DNA methyltransferases, induces hypomethylation, blocks DNA replication, and causes DNA single strand breaks (SSBs). As the PARP inhibitor is expected to affect both DNA repair and transcriptional regulations, we investigated the effect of combinational use of PARP inhibitors on cytotoxicity of 5-aza-dC in human cancer cell lines. The combinational treatment of 5-aza-dC and PARP inhibitor PJ-34 exhibited a stronger cytotoxicity compared with their treatment alone in blood cancer HL-60, U937, and colon cancer HCT116 and RKO cells. Treatment with 5-aza-dC but not PJ-34 caused SSBs in HCT116 cell lines. Global genome DNA demethylation was observed after treatment with 5-aza-dC but not with PJ-34. Notably, in microarray analysis, combinational treatment with PJ-34 and 5-aza-dC caused dissimilar broad changes in gene expression profiles compared with their single treatments in both HCT116 and RKO cells. The profiles of reactivation of silenced genes were also different in combination of PJ-34 and 5-aza-dC and their single treatments. The results suggest that the combinational use of 5-aza-dC and PARP inhibitor may be useful by causing distinct transcriptional profile changes.

Indexed as

5-aza-2′-deoxycytidineDNA methylationmicroarrayPARP inhibitortranscription

Identifiers

PMID36077707
PMCPMC9454563
OpenAlexW4293659819

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.