ArticleBiomolecules2025
Uncovering a Novel Role of ROR1 in the Epigenetic Regulation of Tumor Suppressor Gene CREB3L1 in Triple-Negative Breast Cancer Cells.
Article in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Matrix stiffness induced CREB3L1 activation contributed to skin fibrosis through calcium influx triggered endoplasmic reticulum stress.Cellular and molecular life sciences : CMLS · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
A characteristic of triple-negative breast cancer (TNBC) is the epigenetic regulation of tumor suppressor genes, leading to TNBC heterogeneity and treatment resistance in patients. TNBC exhibits high methylation rates, leading to the silencing of numerous tumor suppressor genes. DNA methyltransferase inhibitors (DNMTis) have shown limited clinical efficacy in TNBC treatment. This study aims to uncover a target that could be used to reverse the epigenetic silencing of tumor suppressor genes in TNBC. The Western blot analysis demonstrated that ROR1 knockdown, an oncofetal gene, reduced DNMT3A and DNMT3B protein expression in the TNBC cell lines MDA-MB-231 and HCC1806, as well as a non-malignant breast cell line, MCF10A. The reduced representation bisulfite sequencing (RRBS) analysis identified differential methylation of CREB3L1 when ROR1 is knocked down in TNBC cell lines. CREB3L1 is a transcription factor that plays tumor-suppressive roles in TNBC and is commonly epigenetically silenced in patients. This study shows that ROR1 requires pSTAT3 activation to upregulate DNMT3A and DNMT3B expression to induce CREB3L1 epigenetic silencing in TNBC. ROR1 knockdown resulted in the re-expression of CREB3L1 in TNBC cells. The data provide evidence that ROR1 inhibition, in combination with DNMTis, could enhance patient outcomes as a therapeutic approach for TNBC.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.