Evidence map›Paper›PMID 40163200›Full record

ReviewMedical oncology (Northwood, London, England)2025

Noncoding RNA (ncRNA)-mediated regulation of TLRs: critical regulator of inflammation in tumor microenvironment.

Tawfeeq Alghazali, Abdulrahman T Ahmed, Uday Abdul-Reda Hussein, Gaurav Sanghvi, Subasini Uthirapathy, Reem Turki Edan, Madan Lal, Debasish Shit, K Satyam Naidu, Ahmed Khudhair Al-Hamairy

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–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

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Noncoding RNAs in periodontitis: Progress and perspectives (Review).International journal of molecular medicine · 2025
    Review
  8. Review
  9. Article
  10. Review
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.

Tawfeeq AlghazaliThe Islamic University, Najaf, Iraq.
Abdulrahman T AhmedCollege of Nursing, University of Al Maarif, Al Anbar, 31001, Iraq. Abdulrahman.dheyab@uoa.edu.iq.
Uday Abdul-Reda HusseinCollege of Pharmacy, University of Al-Ameed, Baghdad, Iraq.
Gaurav SanghviDepartment of Microbiology, Faculty of Science, Marwadi University Research Center, Marwadi University, Rajkot, 360003, Gujarat, India.
Subasini UthirapathyPharmacy Department, Tishk International University, Erbil, Kurdistan Region, Iraq.
Reem Turki EdanDepartment of Medical Laboratories Technology, AL-Nisour University College, Baghdad, Iraq.
Madan LalDepartment of Medicine, National Institute of Medical Sciences, NIMS University Rajasthan, Jaipur, India.
Debasish ShitCentre for Research Impact & Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, 140401, Punjab, India.
K Satyam NaiduDepartment of Chemistry, Raghu Engineering College, Visakhapatnam, Andhra Pradesh, 531162, India.
Ahmed Khudhair Al-HamairyAnesthesia Techniques Department, College of Health and Medical Techniques, Al-Mustaqbal University, 51001, Babylon, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptors (TLRs) are central components of the innate immune system as they recognize molecular patterns associated with pathogens and cellular damage and initiate immune responses using MyD88- and TRIF-dependent pathways. In contrast to being very useful for immune defense, dysregulated TLR signaling may be involved in diseases, such as cancer and autoimmune conditions. In cancer, TLRs create an environment that supports tumorigenesis and growth. In addition to this, a class of multifunctional noncoding RNAs (ncRNAs), including miRNAs, lncRNAs, and circRNAs, regulate gene expression without encoding proteins. MiRNAs regulate gene expression in a fine-tuned manner, while lncRNAs and circRNAs do so via diverse mechanisms. Notably, these ncRNAs interact, where lncRNAs and circRNAs function as competing endogenous RNAs and ceRNA, affecting miRNA activity. This interaction has a vital role in cancer pathology, in influencing that of various oncogenes and tumor suppressors in the tumor microenvironment; hence, modulation of ncRNAs could also be a great promising therapeutic approach. In this context, interplay between TLRs and ncRNAs is of paramount importance as they influence various parameters of the tumor microenvironment. TLR signaling works upon the expression of ncRNAs, while ncRNAs work back to regulate TLR signaling in return. An example of this includes miRNA targeting of components of the TLR; lncRNAs induced by TLR signaling possibly would favor tumor progression. Pharmacological interventions directed toward inhibiting these TLR pathways could be the model to halt malignancy by hampering pro-tumor inflammation and boosting immune responses against neoplasms. Hence, the review will highlight the complicated contrast of ncRNAs and TLRs within human cancer. By connecting the mechanisms, the researchers may study more about tumorigenesis and gather up new, innovative notions regarding therapeutic targeting.

Indexed as

InflammationNeoplasmsRNA, UntranslatedToll-Like ReceptorsTumor MicroenvironmentAnimalsGene Expression Regulation, NeoplasticHumansMicroRNAsRNA, Long NoncodingSignal TransductionMicroRNAsRNA, Long NoncodingRNA, UntranslatedToll-Like ReceptorsCancerCircRNALncRNAMicroRNAToll-like receptor (TLR)

Identifiers

PMID40163200

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.