ArticleInternational journal of molecular sciences2025
Biological Performance and Molecular Mechanisms of Mesyl MicroRNA-Targeted Oligonucleotides in Colorectal Cancer Cells.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- Panel-Wide Screening of Tumour Cells of Diverse Histogenesis for Responsiveness to Silencing of miR-21, miR-17, and miR-155 by Mesyl Phosphoramidate Antisense Oligonucleotides.International journal of molecular sciences · 2026Article
- Targeted Inhibition of Oncogenic microRNAs miR-21, miR-17, and miR-155 Suppresses Tumor Growth and Modulates Immune Response in Colorectal Cancer.Pharmaceutics · 2026Article
- Reversing the Irreversible: miRNA-Targeting Mesyl Phosphoramidate Oligonucleotides Restore Sensitivity to Cisplatin and Doxorubicin of KB-8-5 Epidermoid Carcinoma Cells.Biomedicines · 2025Article
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
Abstract
Colorectal cancer (CRC) remains one of the most aggressive and therapeutically resistant malignancies worldwide. This study examined the molecular mechanisms underlying the anti-oncogenic activity of methanesulfonyl phosphoramidate-modified antisense oligonucleotides (µ-ASOs) targeting miR-21, miR-17, and miR-155, which represent critical oncogenic drivers in CRC. Using human colorectal adenocarcinoma Caco-2 cells transfected with either individual µ-ASOs or their triple combination, we assessed target miRNA downregulation, antiproliferative and anti-migratory activities, and performed extensive proteomic profiling. Protein-protein interaction network analysis of differentially expressed proteins (DEPs) revealed that, beyond modulation of core metabolic processes, each µ-ASO exhibited distinct effects: µ-21 predominantly affected apoptosis, cell cycle, and DNA repair; µ-17 influenced proliferation and chaperone responses; and µ-155 modulated intracellular transport and immune regulation. Combination treatment elicited a unique proteomic signature partially overlapping with monotherapies. The proteomic analysis revealed several validated and putative miRNA-targeted DEPs, including both established and novel candidates in the CRC context: RPL31, CCT2, and CDC37 (miR-21); DNM2, SNRPN, NUP98, and NUP85 (miR-17); as well as RPL17 (miR-155). Expression of these targets correlated with favorable clinical outcomes in CRC patients. This work provides the first comprehensive mechanistic insight into antisense oligonucleotide-mediated miRNA suppression in Caco-2 colorectal adenocarcinoma cells and expands the miRNA target landscape.
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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.