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Carcinogenesis arises when aberrant ncRNA networks initiate malignant transformation and sustain oncogenic changes through epigenetic modifications, shifts in cell identity, failures in genome protection, metabolic changes, and alterations in the tumour microenvironment. Environmental exposures, combined with chronic inflammation, reorganize these networks early on, leading to the formation of premalignant fields and persistent epigenetic changes. The four major ncRNA classes, microRNAs (miRNAs), long noncoding RNAs (lncRNAs), circular RNAs (circRNAs), and PIWI-interacting RNAs (piRNAs) function as either oncogenes or tumour suppressors depending on the specific cancer type. Their stability, cell-type-specific expression, and presence in biofluids make them suitable candidates for biomarker discovery and liquid biopsy applications. Therapeutic strategies now include antisense oligonucleotides, small interfering RNAs, synthetic miRNA mimics, RNA aptamers, and aptamer-siRNA conjugates, which can either inhibit oncogenic ncRNAs or restore tumour-suppressive regulatory networks. CRISPR-based ncRNA modulation, including Cas9-mediated locus editing, CRISPR interference\/activation, and Cas13-mediated transcript targeting, remains largely investigational because delivery, off-target activity, and an incomplete understanding of ncRNA context dependence continue to limit translation. High-throughput sequencing, single-cell transcriptomics, and computational modelling have accelerated the identification of cancer-related ncRNAs and elucidated their biological functions. This review examines how different types of ncRNAs contribute to cancer initiation, progression, and treatment resistance, and assesses their potential as diagnostic markers, prognostic factors, and therapeutic targets.<\/jats:p>","DOI":"10.1093\/carcin\/bgag053","type":"journal-article","created":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T20:01:41Z","timestamp":1787947301000},"source":"Crossref","is-referenced-by-count":0,"title":["The emerging roles of noncoding RNAs in cancer"],"prefix":"10.1093","volume":"47","author":[{"given":"Akanksha","family":"Samuel","sequence":"first","affiliation":[{"name":"Translational Molecular Pathology Department, MD Anderson Cancer Center, University of Texas , Houston, TX 77030 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7427-0578","authenticated-orcid":false,"given":"George A","family":"Calin","sequence":"additional","affiliation":[{"name":"Translational 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