ArticleBiochemical genetics2026
Hsa-miR-526b-5p Regulates the Sensitivity of Colorectal Cancer to 5-Fluorouracil by Targeting TP53 in Organoid Models.
Article in Biochemical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- ALDH1L2 suppresses ferroptosis-associated responses and reduces sunitinib sensitivity in renal cell carcinoma organoids.Biology direct · 2026Article
- Role of non-coding RNA-regulated ferroptosis in colorectal cancer.Cell death discovery · 2025Review
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
This study aimed to explore the mechanisms through which microRNAs (miRNAs) regulate 5-fluorouracil (5-FU) sensitivity in colorectal cancer (CRC) using organoid models. Fresh tissue samples from CRC tumors were collected, and CRC organoids were isolated and cultured. The consistency between CRC organoids and their derived tissues was validated. CRC organoids were treated with 5-FU, and ATP activity was measured. High-throughput sequencing of CRC organoids, combined with Gene Expression Omnibus (GEO) data analysis, was performed to examine miRNA expression following 5-FU treatment. Next, we investigated the cellular function of miR-526b-5p in CRC organoids and cells. Dual-luciferase reporter assays validated the binding of miR-526b-5p to the 3' UTR of TP53 mRNA. We successfully established CRC organoids that exhibited characteristics consistent with their source tissues. 5-FU treatment suppressed the proliferation and ATP activity of CRC organoids. High-throughput sequencing of CRC organoids, combined with GEO data analysis and quantitative reverse transcription polymerase chain reaction (qRT-PCR) validation, revealed that hsa-miR-526b-5p levels were elevated following 5-FU treatment in CRC organoids and cells. Furthermore, hsa-miR-526b-5p was upregulated in CRC tissues compared to adjacent normal tissues, correlating with poor survival in CRC patients. Overexpression of hsa-miR-526b-5p mitigated the inhibitory effects of 5-FU on CRC organoid proliferation, migration, invasion, and ferroptosis. In contrast, silencing of hsa-miR-526b-5p impaired cell function and ferroptosis. Additionally, overexpression of hsa-miR-526b-5p decreased TP53 mRNA and protein levels while increasing the expression of SLC7A11 mRNA and protein. Silencing of hsa-miR-526b-5p resulted in the opposite effect. hsa-miR-526b-5p directly targeted and inhibited TP53 expression. Overexpression of TP53 diminished the promotive effect of hsa-miR-526b-5p on ferroptosis-related proteins GPX4 and SLC7A11, whereas inhibition of TP53 reversed the impact of hsa-miR-526b-5p silencing. Our study demonstrates that hsa-miR-526b-5p targets TP53 to regulate 5-FU sensitivity in CRC through the ferroptosis pathway based on CRC organoid models.
Indexed as
Identifiers
39953363What 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.