Evidence map›Paper›PMID 41562705›Full record

ArticleEpigenomes2026

Fisetin Suppresses the Proliferative and Migratory Behavior of HeLa Cells by Modulating Aberrant Epigenetic Marks (Writers and Erasers).

Nazia Afroze, Reham I Alagal, Lujain A Almousa, Ritu Raina, Prathap Bava, Lizna Mohamed Ali, Tarique Noorul Hasan, Arif Hussain

Abstract read
In one paragraph

Article in Epigenomes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

8 authors.

Nazia AfrozeSchool of Life Sciences, Manipal Academy of Higher Education, Dubai P.O. Box 345050, United Arab Emirates.
Reham I AlagalDepartment of Health Sciences, College of Health and Rehabilitation Sciences, Princess Nourah Bint Abdulrahman University, P.O. Box 84428, Riyadh 11671, Saudi Arabia.ORCID 0000-0002-8515-1574
Lujain A AlmousaDepartment of Health Sciences, College of Health and Rehabilitation Sciences, Princess Nourah Bint Abdulrahman University, P.O. Box 84428, Riyadh 11671, Saudi Arabia.ORCID 0000-0002-7968-418X
Ritu RainaSchool of Life Sciences, Manipal Academy of Higher Education, Dubai P.O. Box 345050, United Arab Emirates.
Prathap BavaSchool of Life Sciences, Manipal Academy of Higher Education, Dubai P.O. Box 345050, United Arab Emirates.
Lizna Mohamed AliDepartment of Microbiology and Immunology, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain P.O. Box 17666, United Arab Emirates.
Tarique Noorul HasanDepartment of Molecular Genetics, PureLab, Sh. Tahnoon Bin Mohammed Medical City (STMC), Al Ain P.O. Box 134808, United Arab Emirates.
Arif HussainSchool of Life Sciences, Manipal Academy of Higher Education, Dubai P.O. Box 345050, United Arab Emirates.ORCID 0000-0002-0851-4845

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe reversible deviant in epigenomic modulations is the highlight of developing new anti-cancer drugs, necessitating the use of fisetin as an epigenetic modifier in the study.

methodsIn silico and molecular studies were performed to analyze the modulatory effect of fisetin on various writers and erasers. Further, whole genome DNA methylation sequencing and expression studies were performed. Global DNA methylation-LINE 1 kit was used to check global DNA methylation. Additionally, the effect of fisetin on migration was evaluated by colony, scratch, and invasion assays and qPCR and protein expression studies of migration-related genes were carried out on HeLa cells.

resultsIn silico studies have supported that fisetin interacts with writers and erasers in their catalytic site and the simulation studies showed minimum fluctuations in energy and temperature over a 10 ns timescale indicating that these complexes are likely to remain stable. Fisetin (20-50 µM) dose-dependently inhibited DNA methyltransferases (DNMT), histone deacetyl transferases (HDAC), histone acetyl transferases (HAT), and histone methyltransferases (HMT) activities at 48 h, with inhibition ranging from 24 to 72% compared to the control. The expression and enzymatic activity of these proteins, along with various H4 and H3 modification marks, were observed to be altered following fisetin treatment at 48 h. Fisetin treatment reduced promoter methylation in various tumor suppressor genes ranging from 15.29% to 76.23% and leading to the corresponding reactivation of important tumor suppressor genes; however, it did not lead to any alteration in the global DNA methylation compared to untreated controls linked with the anti-migratory properties of fisetin as the percentage of migrated cells dropped from ~40% to ~8%.

conclusionsThis study gives a mechanistic insight of fisetin as a potential epigenetic modifier in HeLa cells.

Indexed as

DNA methylationepigenetic modificationepigenomefisetinmethyl sequencing

Identifiers

PMID41562705
PMCPMC12821405

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.