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Emerging Roles of Lncrna Msc-As1 in Cancer: Molecular Mechanisms, Clinical Implications, and Therapeutic Potential Publisher



Mir M ; Kurbanbayeva A ; Ruzieva M ; Yaxshimuratov M ; Mirzayev O ; Khadieva D ; Ebrahimzade M ; Hamzeh S
Authors

Source: Asian Pacific Journal of Cancer Biology Published:2025


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. © 2025 Elsevier B.V., All rights reserved.
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