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<p>Non-coding RNAs (ncRNAs) influence gene expression and diverse physiological and pathological processes. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) play roles in cancer and neurodegenerative diseases. LncRNAs, such as <i>HOTAIR</i>,<i> MALAT1</i>, and <i>NEAT1</i>, regulate chromatin remodeling through histone modification. Dysregulated expression leads to oncogenesis and neuronal dysfunction. Conversely, miRNAs such as miR-21 and miR-155, as post-transcriptional regulators, act in oncogenic signaling and neuroinflammation. MiR-21 targets <i>PTEN</i> and <i>PDCD4</i>, leading to aberrant activation of the PI3K/AKT and NF-κB pathways, thereby promoting cancer cell proliferation, while influencing neuronal apoptosis and neuroprotection. Similarly, miR-155 modulates SHIP1 and SOCS1 through AKT and JAK/STAT pathways in both cancer and neurodegenerative contexts. The convergence of these signaling cascades reveals a shared molecular framework that links tumor progression to neurodegeneration. Understanding the intricate lncRNA–miRNA–mRNA regulatory networks provide valuable insights into disease mechanisms and clinical applications regarding ncRNAs as biomarkers. Further research integrating transcriptomics, functional genomics, and therapeutic delivery systems is essential to harness the full diagnostic and therapeutic potential of ncRNAs.</p>

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Functional dynamics of lncRNAs and miRNAs in cancer metabolism and neuroinflammation

  • 期刊论文

  • 发表日期：

    2026年5月16日

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  • Ananya Das,
  • Afsana Bhuiyan

摘要

Non-coding RNAs (ncRNAs) influence gene expression and diverse physiological and pathological processes. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) play roles in cancer and neurodegenerative diseases. LncRNAs, such as HOTAIR, MALAT1, and NEAT1, regulate chromatin remodeling through histone modification. Dysregulated expression leads to oncogenesis and neuronal dysfunction. Conversely, miRNAs such as miR-21 and miR-155, as post-transcriptional regulators, act in oncogenic signaling and neuroinflammation. MiR-21 targets PTEN and PDCD4, leading to aberrant activation of the PI3K/AKT and NF-κB pathways, thereby promoting cancer cell proliferation, while influencing neuronal apoptosis and neuroprotection. Similarly, miR-155 modulates SHIP1 and SOCS1 through AKT and JAK/STAT pathways in both cancer and neurodegenerative contexts. The convergence of these signaling cascades reveals a shared molecular framework that links tumor progression to neurodegeneration. Understanding the intricate lncRNA–miRNA–mRNA regulatory networks provide valuable insights into disease mechanisms and clinical applications regarding ncRNAs as biomarkers. Further research integrating transcriptomics, functional genomics, and therapeutic delivery systems is essential to harness the full diagnostic and therapeutic potential of ncRNAs.