REVIEW article
Front. Cell Dev. Biol.
Sec. Cancer Cell Biology
This article is part of the Research TopicEpigenetic Regulation in Cancer: Mechanisms, Implications, and Therapeutic InterventionsView all 4 articles
In-silico pharmacological insights into the therapeutic potential of microRNAs for microplastic-associated cancers
Provisionally accepted
Akmaral Baspokova1
Afshin Zare2
Nadiar Maratovich Mussin1
Nader Tanideh3
Kulyash R. Zhilisbayeva1Ramazon Safarzoda Sharoffidin4Roza Suleimenova5Gulden Yelgondina6Akmeiir E. Kaliyeva1Aigerim A. Umbetova1Ainur N. Zinaliyeva1
Amin Tamadon1*- 1West Kazakhstan Marat Ospanov State Medical University, Aktobe, Fars province, Kazakhstan
- 2Taipei Medical University, Taipei City, Taiwan
- 3Shiraz University of Medical Sciences, Shiraz, Iran
- 4Avicenna Tajik State Medical University, Dushanbe, Tajikistan
- 5Astana Medical University, Astana, Kazakhstan
- 6Asfendiyarov Kazakh National Medical University, Almaty, Kazakhstan
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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 in vivo testing in MP-exposed models. Collectively, our results nominate miRNAs as candidate tools to interrogate and potentially mitigate MP-associated carcinogenic mechanisms.
Keywords: Microplastics, MicroRNAs, Cancer, therapy resistance, in silico, RNAhybrid
Received: 05 Sep 2025; Accepted: 29 Oct 2025.
Copyright: © 2025 Baspokova, Zare, Mussin, Tanideh, Zhilisbayeva, Safarzoda Sharoffidin, Suleimenova, Yelgondina, Kaliyeva, Umbetova, Zinaliyeva and Tamadon. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Amin Tamadon, amintamaddon@yahoo.com
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