ArticleFrontiers in medicine2025
Hsa_circ_0020095 modulates chemoresistance of CRC in a PDO model.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Global research trends and hotspots of colorectal cancer organoids: a bibliometric insight and visualization analysis via multiple databases.Frontiers in oncology · 2026Pooled it
- Mechanisms and advances of drug resistance in colorectal cancer: A systematic overview of multi-layered regulatory networks.Translational oncology · 2026Review
- Enterococcus hirae Y-HS Alleviates Ulcerative Colitis by Activating PXR/Nrf2-mediated Metabolic-immune Crosstalk.Probiotics and antimicrobial proteins · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Colorectal cancer (CRC) is the third most common malignant tumor type all over the world with high mortality. Chemoresistance of CRC leads to treatment failure and disease aggravation. We previously identified Hsa_circ_0020095 as a novel oncogene to promote progression and cisplatin-resistance in colon cancers by modulating the miR-487a-3p/SOX9 axis. Methods: Patient-derived organoids (PDOs) were generated from CRC patients and validated by H&E staining, immunohistochemistry (IHC), and whole exome sequencing (WES). Hsa_circ_0020095 was knocked down in PDOs by shRNA and the inhibition of hsa_circ_0020095 was determined using RT-qPCR. The RNA samples analyzed separately, and then pooled together for KEGG and GO analyses. The effects of knocking down hsa_circ_0020095 on drug-resistance of PDOs were examined using CellTiter-Glo Results: Five organoid lines were successfully established from CRC patients using surgically resected tumor samples. PDOs resembled their parental tumor tissues in morphology, histopathology, and genetic alterations. Silencing of circ_0020095 resulted in remarkable inhibition of hsa_circ_0020095 in PDOs and reversed the resistance of PDOs to 5-FU and oxaliplatin. Mechanistically, hsa_circ_0020095 may function by modulating key pathways and biological functions involved in pathophysiological processes in CRC. Conclusion: Hsa_circ_0020095 modulates chemoresistance of CRC, which could potentially be explored as a therapeutic target for CRC treatment.
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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.