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Emerging Roles of lncRNA MSC-AS1 in Cancer: Molecular Mechanisms, Clinical Implications, and Therapeutic Potential

M. A. MirDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, IranAsel KurbanbayevaAssociate Professor, Doctor of Philosophy in Pedagogical Sciences, Head of the Department of Chemical Engineering and Environmental Protection of Nukus State Technical University, UzbekistanMukhayya RuzievaDepartment of sport and psychology, Mamun university, Khiva UzbekistanMurodjon YaxshimuratovDepartment of Chemistry, Urgench State University, Urgench UzbekistanOtabek MirzayevTeacher, Department of Transport Systems, Urgench State University named after Abu Rayhan Biruni, Urgench, Republic of UzbekistanDora KhadievaAssistаnt of the Department of “Infectious Diseases and Infectious Diseases of Children”, Bukhara State Medical Institute Named after Abu Ali Ibn Sino, Bukhara, UzbekistanMohammadreza EbrahimzadeDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, IranSoroosh HamzehIran University of Medical Sciences, School of Medicine, Tehran, Iran
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Abstract

Overview: Long non-coding RNAs (lncRNAs) are key regulators of tumor biology, affecting proliferation, apoptosis, metastasis, and treatment resistance. Among them, Musculin Antisense RNA 1 (MSC-AS1) has attracted increasing attention for its oncogenic roles across multiple cancers. This review summarizes current knowledge on MSC-AS1, emphasizing molecular mechanisms, clinical relevance, and therapeutic potential. Methods: A comprehensive literature search of PubMed, Scopus, and Web of Science identified studies published 2015–2024 that investigated MSC-AS1 in cancer. Eligible articles examined its functional roles, implicated signaling pathways, regulatory interactions (e.g., lncRNA–miRNA–mRNA axes), and diagnostic, prognostic, or therapeutic implications. Results: Evidence consistently shows that MSC-AS1 is frequently upregulated in gastric, hepatic, pancreatic, and colorectal cancers. Mechanistically, MSC-AS1 contributes to tumor progression mainly through lncRNA–miRNA–mRNA regulatory networks, promoting malignant phenotypes and therapeutic resistance. Clinically, elevated MSC-AS1 expression correlates with poor prognosis, supporting its utility as a biomarker for diagnosis and prognosis and as a candidate target for precision oncology. Conclusion: MSC-AS1 functions as an oncogenic lncRNA across multiple gastrointestinal and hepatobiliary malignancies, driving disease through competitive regulatory networks and associating with adverse outcomes and resistance. Current evidence positions MSC-AS1 as a promising biomarker and a potential therapeutic target; future work should validate its clinical performance and evaluate targeted interventions against MSC-AS1-mediated pathways.

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