ReviewFrontiers in cell and developmental biology2025
In-silico pharmacological insights into the therapeutic potential of microRNAs for microplastic-associated cancers.
Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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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.
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0 citing papers in PubMed.
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microplastics (MPs) are increasingly implicated in cancer biology through effects on gene expression, stress responses, and treatment susceptibility; however, causal links remain provisional. We systematically screened PubMed and Google Scholar (through September 2025) to identify cancer-related genes reported to be altered by MP exposure and then evaluated microRNAs (miRNAs) with anticancer activity that may target those genes. Mature miRNA sequences were retrieved from RNAcentral and assessed against MP-altered genes using RNAhybrid for target-site prediction and minimum free-energy (mfe) hybridization. MPs were reported to modulate genes across multiple tumor types-including breast, gastric, liver, lung, colorectal, cervical, pancreatic, and skin. In silico analyses identified candidate miRNAs with favorable mfe values for these targets, including miR-483-3p, miR-365, miR-331-3p, miR-138-5p, miR-760, miR-1-3p, miR-665, miR-490-3p, miR-370-3p, miR-520a, miR-638, miR-559, miR-532-3p, miR-593-5p, and miR-29b. These interactions suggest putative avenues to counter MP-associated oncogenic programs and therapy resistance. Because mfe predictions do not establish functional regulation, all findings should be interpreted as hypothesis-generating. Priorities for validation include reporter assays, gene/protein modulation, phenotypic rescue, and
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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.