Evidence map›Paper›PMID 35008411›Full record

ArticleCancers2022

Epigenetic Priming with Decitabine Augments the Therapeutic Effect of Cisplatin on Triple-Negative Breast Cancer Cells through Induction of Proapoptotic Factor NOXA.

Wataru Nakajima, Kai Miyazaki, Masahiro Sakaguchi, Yumi Asano, Mariko Ishibashi, Tomoko Kurita, Hiroki Yamaguchi, Hiroyuki Takei, Nobuyuki Tanaka

Open access · goldAbstract read
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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Wataru NakajimaDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo 113-0033, Japan.
Kai MiyazakiDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo 113-0033, Japan.
Masahiro SakaguchiDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo 113-0033, Japan.ORCID 0000-0002-1303-5494
Yumi AsanoDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo 113-0033, Japan.
Mariko IshibashiDepartment of Microbiology and Immunology, Nippon Medical School, Tokyo 113-0033, Japan.ORCID 0000-0001-8292-9283
Tomoko KuritaDepartment of Breast Surgery and Oncology, Nippon Medical School, Tokyo 113-0033, Japan.ORCID 0000-0002-6139-5996
Hiroki YamaguchiDepartment of Hematology, Nippon Medical School, Tokyo 113-0033, Japan.ORCID 0000-0002-0571-7495
Hiroyuki TakeiDepartment of Breast Surgery and Oncology, Nippon Medical School, Tokyo 113-0033, Japan.
Nobuyuki TanakaDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo 113-0033, Japan.
Nippon Medical School · JP

Funding

Japan Society for the Promotion of Science 17H04554Japan Society for the Promotion of Science JP16K11161
6 · The paper itself

Abstract

Epigenetic alterations caused by aberrant DNA methylation have a crucial role in cancer development, and the DNA-demethylating agent decitabine, is used to treat hematopoietic malignancy. Triple-negative breast cancers (TNBCs) have shown sensitivity to decitabine; however, the underlying mechanism of its anticancer effect and its effectiveness in treating TNBCs are not fully understood. We analyzed the effects of decitabine on nine TNBC cell lines and examined genes associated with its cytotoxic effects. According to the effect of decitabine, we classified the cell lines into cell death (D)-type, growth inhibition (G)-type, and resistant (R)-type. In D-type cells, decitabine induced the expression of apoptotic regulators and, among them, NOXA was functionally involved in decitabine-induced apoptosis. In G-type cells, induction of the cyclin-dependent kinase inhibitor, p21, and cell cycle arrest were observed. Furthermore, decitabine enhanced the cytotoxic effect of cisplatin mediated by NOXA in D-type and G-type cells. In contrast, the sensitivity to cisplatin was high in R-type cells, and no enhancing effect by decitabine was observed. These results indicate that decitabine enhances the proapoptotic effect of cisplatin on TNBC cell lines that are less sensitive to cisplatin, indicating the potential for combination therapy in TNBC.

Indexed as

apoptosiscisplatindecitabineDNA methylationdrug combinationNOXAtriple-negative breast cancer

Identifiers

PMID35008411
PMCPMC8749981
OpenAlexW4206414571

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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.