Oncogenic Long Non-Coding RNAs in Cancer: Comparative Analysis of HOTAIR and MINCR in Modulating Transcriptional and Post Transcriptional Pathways
DOI:
https://doi.org/10.61919/0x61k339Keywords:
long non-coding RNA; HOTAIR; MINCR; MYC; chromatin remodelling; epigenetics; transcriptional regulation; cancer prognosis; chemoresistance.Abstract
Background: Long non-coding RNAs (lncRNAs) have emerged as key regulators of gene expression in cancer, modulating chromatin architecture, transcriptional programs, and post-transcriptional processes. HOTAIR and MINCR are two prototypical oncogenic lncRNAs that have been independently linked to tumour progression, metastasis, and therapy resistance, but their comparative roles in shaping transcriptional and post-transcriptional oncogenic pathways remain incompletely synthesised. Objective: To compare the molecular functions of HOTAIR and MINCR in human malignancies, focusing on their roles in transcriptional and post-transcriptional regulation, oncogenic signalling, and clinically relevant outcomes, and to evaluate their potential as prognostic biomarkers and therapeutic targets. Methods: A narrative comparative review was conducted using PubMed, Embase, Web of Science, and Google Scholar up to December 2024 to identify mechanistic, translational, and clinical studies of HOTAIR and MINCR in cancer. Eligible studies included experimental models, clinical cohorts, and meta-analyses reporting molecular mechanisms, cellular phenotypes, or associations with stage, treatment response, or survival. Data on chromatin remodelling, MYC signalling, microRNA interactions, and clinical endpoints were extracted and summarised in comparative tables. Results: HOTAIR predominantly functions as an epigenetic scaffold that recruits PRC2 and LSD1/CoREST complexes to enforce transcriptional silencing of tumour suppressor genes, promoting EMT, metastasis, and chemoresistance. Meta-analytic data show that high HOTAIR expression approximately doubles the hazard of death across multiple cancers. MINCR is a MYC-induced lncRNA that amplifies MYC transcriptional programs, enhances expression of cell-cycle regulators, and promotes proliferation and survival, particularly in MYC-positive lymphomas and NSCLC. MINCR is consistently upregulated in tumour tissues, and its silencing reduces proliferation and induces apoptosis, although large pooled survival analyses remain limited. Conclusion: HOTAIR and MINCR exemplify distinct yet convergent oncogenic lncRNA mechanisms—epigenetic suppression and transcriptional amplification—that cooperatively drive malignant progression and therapy resistance. HOTAIR currently has stronger prognostic validation, whereas MINCR represents a promising biomarker and target in MYC-driven cancers. Integrating both lncRNAs into biomarker panels and therapeutic strategies may enhance precision in cancer diagnosis, risk stratification, and targeted treatment.
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Copyright (c) 2025 Arfat Hussain, Zainab Butt, Tehmina Shoukat, Hafiz Ayaz Ahmad (Author)
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