Evidence map›Paper›PMID 40643648›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2025

LncRNA-Histone Modification Crosstalk: Orchestrating Cancer Pathobiology.

Saade Abdalkareem Jasim, Harikumar Pallathadka, Ahmed Hjazi, Gaurav Sanghvi, Rekha M M, Mohit Agarwal, Renu Arya, Mohammed Qasim Alasheqi, Abed J Kadhim, Muthena Kariem

Abstract readReview
PubMed Publisher
In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
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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

10 authors.

Saade Abdalkareem JasimMedical Laboratory Techniques Department, College of Health and Medical Technology, University of Al-Maarif, Anbar, Iraq. saad.a.j.anbar@gmail.com.
Harikumar PallathadkaManipur International University, Imphal, Manipur, India. pallathadkaharikumar1402@gmail.com.
Ahmed HjaziDepartment of Medical Laboratory, College of Applied Medical Sciences, Prince Sattam Bin Abdulaziz University, Al-Kharj, Saudi Arabia.
Gaurav SanghviDepartment of Microbiology, Faculty of Science, Marwadi University Research Center, Marwadi University, Rajkot, 360003, Gujarat, India.
Rekha M MDepartment of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to Be University), Bangalore, Karnataka, India.
Mohit AgarwalDepartment of Pharmaceutical Chemistry, NIMS Institute of Pharmacy, NIMS University Rajasthan, Jaipur, 302131, India.
Renu AryaChandigarh Pharmacy College, Chandigarh Group of Colleges-Jhanjeri, Mohali, 140307, Punjab, India.
Mohammed Qasim AlasheqiCollege of Pharmacy, National University of Science and Technology, Dhi Qar, Iraq.
Abed J KadhimDepartment of Medical Engineering, Al-Nisour University College, Baghdad, Iraq.
Muthena KariemDepartment of Medical Analysis, Medical Laboratory Technique College, the Islamic University, Najaf, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) and histone modifications are key epigenetic regulators in cancer pathobiology. This review delves into the crosstalk between lncRNAs and histone modifications relevant to tumor initiation and development in a detailed manner. Histone modifications (e.g., methylation, acetylation, phosphorylation, and ubiquitination) play key roles in chromatin structure and gene expression, involved in such cellular processes as proliferation, metastasis, and drug resistance. These lncRNAs have a variety of mechanisms of action, such as signaling, scaffolding, decoying, and guiding to modify critical cellular pathways. They recruit histone methyltransferases, demethylases, acetyltransferases, and deacetylases to specific regions of genomic transcription regulation, thereby changing certain histone-modifying marks that affect gene expression. The abnormal expression and activities of lncRNAs such as HOTAIR, MALAT1, LINC00152, and SNHG1 are associated with tumor initiation, progression, and metastasis in various cancers. Therefore, these molecules are candidates for diagnostic and prognostic biomarkers, making non-invasive detection and prediction possible. LncRNA-related histone modifications also serve as an attractive candidate for future therapeutic targets in cancer. Antisense oligonucleotides, small molecule inhibitors, and RNA interference are some of the strategies currently being investigated to dislodge the interactions between lncRNAs and histone-modifying enzymes, and they represent novel strategies for cancer therapy. This review summarizes recent advances in understanding lncRNA-histone modification crosstalk and its translation to the clinic for precision oncotherapy.

Indexed as

HistonesNeoplasmsRNA, Long NoncodingAnimalsEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansHistonesRNA, Long NoncodingCancerEpigeneticHistonesLncRNAPathology

Identifiers

PMID40643648

What OpenQuestion holds

Textmetadata
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.