ReviewHeliyon2024
The functional roles of competitive endogenous RNA (ceRNA) networks in apoptosis in human cancers: The circRNA/miRNA/mRNA regulatory axis and cell signaling pathways.
Review in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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.
Who cites it
9 citing papers in PubMed.
- Identification of a Circular RNA as a Potential Diagnostic and Prognostic Biomarker in Breast Cancer Through Integrated Bioinformatic and Experimental Analyses.Analytical science advances · 2026Article
- Metabolic remodeling by circular RNAs in gastric tumorigenesis: From mechanisms to biomarker discovery (Review).International journal of oncology · 2026Review
- Multi Omics Integration in Colorectal Cancer: From Molecular Insights to Precision Oncology.Cancers · 2026Review
- Hsa_circ_0002111 implicates KTC-1 cell motility and modulates migration and invasion via miR-432-5p/CDKN2B axis.Scientific reports · 2026Article
- Effect of targeted regulation of miR-499a-5p/integrin β1 by circ_001567 on malignant progression of gastric cancer cells.Journal of molecular histology · 2026Article
- Circ_0041150 inhibits proliferation of pancreatic adenocarcinoma cells by regulating triglyceride accumulation via the miR-1178-3p/AADAC axis.Discover oncology · 2026Article
- Faberidilactone A, a Sesquiterpene Dimer, Inhibits Hepatocellular Carcinoma Progression Through Apoptosis, Ferroptosis, and Anti-Metastatic Mechanisms.Molecules (Basel, Switzerland) · 2025Article
- The functional roles of deoxyelephantopin potential target circTNPO3 in regulating pancreatic cancer malignant phenotype and gemcitabine chemoresistance via miR-188-5p/CDCA3/TRAF2-mediated remodeling of NF-κB signaling pathway.Frontiers in pharmacology · 2025Article
- The role of circRNAs in NScience progressReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Circular RNAs are noncoding RNAs with circular conformation mainly due to backsplicing event. CircRNAs can potentially impact cell biological processes by interacting with cell signaling pathways. Numerous circRNAs have been found to be aberrantly expressed in a variety of cancers. These RNAs can act as ceRNA (competitive endogenous RNA) by sponging certain miRNAs to form circRNA/miRNA/mRNA networks. Dysregulation of ceRNA networks may lead to dysfunctions in various cell pathways, which modulate apoptosis-associated genes and ultimately result in cancer progression. Since disruption of apoptosis is one of the leading causes of cancer development, one approach for cancer treatment is to drive cells toward apoptosis. In this review, we present a summary of studies on the role of ceRNA networks in cellular signaling pathways that regulate apoptosis; these networks are suggested to be potential biomarkers for cancer treatment.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.