Evidence map›Paper›PMID 40138110›Full record

ArticleBulletin of experimental biology and medicine2025

GC-Reach DNA Fragments Reduce the Expression of Survival Genes in MCF7 Breast Carcinoma Cells: TLR9/MyD88/NF-κB Signaling Pathway as a Potential Target for Cancer Therapy.

E M Malinovskaya, G V Shmarina, E S Ershova, L V Kameneva, N N Veiko, V P Veiko, M S Konkova, P A Bobrovsky, E A Kozhina, P E Umriukhin and 6 more

Abstract read
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Article in Bulletin of experimental biology and medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

E M MalinovskayaResearch Centre for Medical Genetics, Moscow, Russia.
G V ShmarinaResearch Centre for Medical Genetics, Moscow, Russia.
E S ErshovaResearch Centre for Medical Genetics, Moscow, Russia.
L V KamenevaResearch Centre for Medical Genetics, Moscow, Russia.
N N VeikoResearch Centre for Medical Genetics, Moscow, Russia.
V P VeikoResearch Centre for Medical Genetics, Moscow, Russia.
M S KonkovaResearch Centre for Medical Genetics, Moscow, Russia.
P A BobrovskyLopukhin Federal Research and Clinical Center of Physical-Chemical Medicine, Federal Medical-Biological Agency of Russia, Moscow, Russia.
E A KozhinaResearch Centre for Medical Genetics, Moscow, Russia.
P E UmriukhinResearch Centre for Medical Genetics, Moscow, Russia. pavelum@mail.ru.
V N LazarevLopukhin Federal Research and Clinical Center of Physical-Chemical Medicine, Federal Medical-Biological Agency of Russia, Moscow, Russia.
A Y AsanovI. M. Se-chenov First Moscow State Medical University, Ministry of Health of the Russian Federation (Sechenov University), Moscow, Russia.
T M RozhnovaI. M. Se-chenov First Moscow State Medical University, Ministry of Health of the Russian Federation (Sechenov University), Moscow, Russia.
V N NikolenkoI. M. Se-chenov First Moscow State Medical University, Ministry of Health of the Russian Federation (Sechenov University), Moscow, Russia.
M Y SinelnikovI. M. Se-chenov First Moscow State Medical University, Ministry of Health of the Russian Federation (Sechenov University), Moscow, Russia.
S V KostyukResearch Centre for Medical Genetics, Moscow, Russia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell-free DNA (cfDNA) attracts increasing attention not only as a diagnostic tool for tumor resistance to cytostatic therapy, but also as an active participant of the tumor process. GC-rich DNA accumulates in the cfDNA pool and stimulates TLR9/MyD88/NF-κB signaling, thereby increasing the expression of genes responsible for viability of cancer cells. We studied the effect of GC-DNA on the transcriptional activity of survival genes in wild-type MCF7 cells (wt MCF7) and TLR9 gene knockout MCF7 cells (TLR9-/- MCF7). It was shown that, in contrast to wt MCF7 cell cultures, TLR9-/- MCF7 cells responded to stimulation with GC-DNA fragments by a decrease in the activity of TLR9/MyD88/NF-κB signaling cascade and a decline in survival gene expression. Our data indicate that TLR9/MyD88/NF-κB signaling cascade components may be considered as potential targets for cancer therapy.

Indexed as

Breast NeoplasmsMyeloid Differentiation Factor 88NF-kappa BToll-Like Receptor 9Cell SurvivalFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsSignal TransductionMYD88 protein, humanMyeloid Differentiation Factor 88NF-kappa BTLR9 protein, humanToll-Like Receptor 9adaptationcell-free DNA (cfDNA)TLR9/MyD88/NF-κB signaling pathwaytumor

Identifiers

PMID40138110

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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.