Evidence mapPaperPMID 41604098Full record

ReviewDiscover oncology2026

MicroRNA-mediated modulation of cancer-associated fibroblasts in HER2-positive breast tumor microenvironment: a comprehensive review.

Mustafa T Ardah, Waleed K Abdulsahib, Hasanain Amer Naji, S Renuka Jyothi, Samir Sahoo, J Bethanney Janney, Vipasha Sharma, Aashna Sinha, Mohigul Kholiyeva

Abstract readReview
In one paragraph

Review in Discover oncology, 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

9 authors.

Mustafa T ArdahFaculty of Allied Medical Sciences, Hourani Center for Applied Scientific Research, Al-Ahliyya Amman University, Amman, Jordan.
Waleed K AbdulsahibDepartment of Pharmacology and Toxicology, College of Pharmacy, Al Farahidi University, Baghdad, Iraq. waleedk.abdulsahib@uoalfarahidi.edu.iq.ORCID http://orcid.org/0000-0002-8851-5783
Hasanain Amer NajiCollege of Pharmacy, Al-Turath University, Baghdad, Iraq.
S Renuka JyothiDepartment of Biotechnology and Genetics, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India.
Samir SahooDepartment of General Medicine, IMS and SUM Hospital, Siksha 'O' Anusandhan, Bhubaneswar, Odisha, 751003, India.
J Bethanney JanneyDepartment of Biomedical, Sathyabama Institute of Science and Technology, Chennai, Tamil Nadu, India.
Vipasha SharmaDepartment of Biotechnology, University Institute of Biotechnology, Chandigarh University, Mohali, Punjab, India.
Aashna SinhaSchool of Applied and Life Sciences, Division of Research and Innovation, Uttaranchal University, Dehradun, Uttarakhand, India.
Mohigul KholiyevaDepartment of Medicine, Termez University of Economics and Serviсe, Termez, Uzbekistan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intricate interplay within the tumor microenvironment (TME) significantly dictates the trajectory of cancer progression and therapeutic response. In HER2-positive breast cancer, a particularly aggressive subtype, cancer-associated fibroblasts (CAFs) emerge as pivotal stromal components, actively orchestrating malignant behaviors. Concurrently, microRNAs (miRNAs), small non-coding RNAs, serve as potent post-transcriptional regulators and critical mediators of intercellular communication, often encapsulated within exosomes. This review provides a comprehensive analysis of the reciprocal miRNA-mediated modulation between HER2-positive breast cancer cells and CAFs. It elucidates how tumor cell-derived miRNAs reprogram normal fibroblasts into pro-tumorigenic CAFs, and how CAF-derived miRNAs, in turn, influence HER2-positive cancer cell proliferation, invasion, metastasis, and crucially, resistance to HER2-targeted therapies. Understanding this dynamic axis reveals a self-sustaining feedback loop that drives disease advancement and therapeutic evasion. This synthesis underscores the immense potential of targeting these complex miRNA-CAF interactions as a novel strategy for diagnostic, prognostic, and therapeutic interventions, aiming to overcome the persistent challenge of resistance in HER2-positive breast cancer.

Indexed as

Cancer-associated fibroblastsHER2-positive breast cancerMicroRNAsTherapeutic resistanceTumor microenvironment

Identifiers

PMID41604098
PMCPMC12923699

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.