Evidence map›Paper›PMID 26161119›Full record

ArticleEvidence-based complementary and alternative medicine : eCAM2015

Sulforaphane Reverses the Expression of Various Tumor Suppressor Genes by Targeting DNMT3B and HDAC1 in Human Cervical Cancer Cells.

Munawwar Ali Khan, Madhumitha Kedhari Sundaram, Amina Hamza, Uzma Quraishi, Dian Gunasekera, Laveena Ramesh, Payal Goala, Usama Al Alami, Mohammad Zeeshan Ansari, Tahir A Rizvi and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Evidence-based complementary and alternative medicine : eCAM, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Article
  3. DNMT Enzymes and Their Impact on Cervical Cancer: A State-of-the-Art Review.International journal of molecular sciences · 2025
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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

12 authors at 3 institutions in 2 countries.

Munawwar Ali KhanDepartment of Natural Science and Public Health, College of Sustainability Sciences & Humanities, Zayed University, P.O. Box 19282, Dubai, UAE.
Madhumitha Kedhari SundaramSchool of Life Sciences, Manipal University, P.O. Box 345050, Dubai, UAE.
Amina HamzaSchool of Life Sciences, Manipal University, P.O. Box 345050, Dubai, UAE.
Uzma QuraishiSchool of Life Sciences, Manipal University, P.O. Box 345050, Dubai, UAE.
Dian GunasekeraSchool of Life Sciences, Manipal University, P.O. Box 345050, Dubai, UAE.
Laveena RameshSchool of Life Sciences, Manipal University, P.O. Box 345050, Dubai, UAE.
Payal GoalaDepartment of Natural Science and Public Health, College of Sustainability Sciences & Humanities, Zayed University, P.O. Box 19282, Dubai, UAE.
Usama Al AlamiDepartment of Natural Science and Public Health, College of Sustainability Sciences & Humanities, Zayed University, P.O. Box 19282, Dubai, UAE.
Mohammad Zeeshan AnsariSchool of Life Sciences, Manipal University, P.O. Box 345050, Dubai, UAE.
Tahir A RizviDepartment of Microbiology & Immunology, Faculty of Medicine and Health Sciences, United Arab Emirates University, P.O. Box 17666, Al Ain, UAE.
Chhavi SharmaSchool of Life Sciences, Manipal University, P.O. Box 345050, Dubai, UAE.
Arif HussainSchool of Life Sciences, Manipal University, P.O. Box 345050, Dubai, UAE.
Manipal Academy of Higher Education · INZayed University · AEUnited Arab Emirates University · AE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sulforaphane (SFN) may hinder carcinogenesis by altering epigenetic events in the cells; however, its molecular mechanisms are unclear. The present study investigates the role of SFN in modifying epigenetic events in human cervical cancer cells, HeLa. HeLa cells were treated with SFN (2.5 µM) for a period of 0, 24, 48, and 72 hours for all experiments. After treatment, expressions of DNMT3B, HDAC1, RARβ, CDH1, DAPK1, and GSTP1 were studied using RT-PCR while promoter DNA methylation of tumor suppressor genes (TSGs) was studied using MS-PCR. Inhibition assays of DNA methyl transferases (DNMTs) and histone deacetylases (HDACs) were performed at varying time points. Molecular modeling and docking studies were performed to explore the possible interaction of SFN with HDAC1 and DNMT3B. Time-dependent exposure to SFN decreases the expression of DNMT3B and HDAC1 and significantly reduces the enzymatic activity of DNMTs and HDACs. Molecular modeling data suggests that SFN may interact directly with DNMT3B and HDAC1 which may explain the inhibitory action of SFN. Interestingly, time-dependent reactivation of the studied TSGs via reversal of methylation in SFN treated cells correlates well with its impact on the epigenetic alterations accumulated during cancer development. Thus, SFN may have significant implications for epigenetic based therapy.

Identifiers

PMID26161119
PMCPMC4487331
OpenAlexW1602155627

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Registered trials

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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.