Evidence map›Paper›PMID 40826481›Full record

ReviewEuropean journal of medical research2025

Circular RNAs: key regulators of paclitaxel sensitivity and resistance in cancer.

Zahra Tajik, Soudeh Ghafouri-Fard

Abstract readReview
In one paragraph

Review in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. 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

2 authors.

Zahra TajikStudent Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Soudeh Ghafouri-FardDepartment of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran. s.ghafourifard@sbmu.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paclitaxel remains a cornerstone of cancer therapy, yet resistance significantly limits its clinical efficacy. Emerging evidence implicates circular RNAs (circRNAs) as key regulators of paclitaxel resistance, offering potential biomarkers and therapeutic targets. This review synthesizes current knowledge on circRNA-mediated resistance mechanisms, categorizing their roles as promoters or suppressors of chemoresistance. We highlight two major pathways-miRNA sponging and protein interactions-through which circRNAs alter drug sensitivity. Moreover, we focus on enhancement of epithelial-mesenchymal transition and modulation of autophagy as two significant downstream pathways influenced by the established primary mechanisms. Notably, our analysis reveals context-dependent dualities, where certain circRNAs exert opposing effects in different cancers, underscoring the need for tissue-specific therapeutic strategies. Furthermore, we identify critical gaps in understanding circRNA regulatory networks and their clinical translatability. By evaluating circRNA signatures associated with paclitaxel response, this review proposes a framework for biomarker development and combination therapies to circumvent resistance. Our findings emphasize the urgency of functional studies and standardized profiling methods to harness circRNAs for personalized oncology.

Indexed as

Antineoplastic Agents, PhytogenicDrug Resistance, NeoplasmNeoplasmsPaclitaxelRNA, CircularBiomarkers, TumorEpithelial-Mesenchymal TransitionHumansAntineoplastic Agents, PhytogenicBiomarkers, TumorPaclitaxelRNA, CircularCircularDrug resistanceLong noncodingNeoplasmPaclitaxelRNA

Identifiers

PMID40826481
PMCPMC12359881

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.