Unraveling the role of LncRNAs in glioblastoma progression: insights into signaling pathways and therapeutic potential

Metab Brain Dis. 2024 Nov 26;40(1):42. doi: 10.1007/s11011-024-01456-y.

Abstract

Glioblastoma (GBM) is one of the most aggressive types of brain cancer, characterized by its poor prognosis and low survival rate despite current treatment modalities. Because GBM is lethal, clarifying the pathogenesis's underlying mechanisms is important, which are still poorly understood. Recent discoveries in the fields of molecular genetics and cancer biology have demonstrated the critical role that non-coding RNAs (ncRNAs), especially long non-coding RNAs (lncRNAs), play in the molecular pathophysiology of GBM growth. LncRNAs are transcripts longer than 200 nucleotides that do not encode proteins. They are significant epigenetic modulators that control gene e expression at several levels. Their dysregulation and interactions with important signaling pathways play a major role in the malignancy and development of GBM. The increasing role of lncRNAs in GBM pathogenesis is thoroughly examined in this review, with particular attention given to their regulation mechanisms in key signaling pathways such as PI3K/AKT, Wnt/β-catenin, and p53. It also looks into lncRNAs' potential as new biomarkers and treatment targets for GBM. In addition, the study discusses the difficulties in delivering lncRNA-based medicines across the blood-brain barrier and identifies areas that need more research to advance lncRNA-oriented treatments for this deadly cancer.

Keywords: Glioblastoma; LncRNAs; PI3K/AKT; Therapeutic approaches; Wnt/β-catenin.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain Neoplasms* / drug therapy
  • Brain Neoplasms* / genetics
  • Brain Neoplasms* / metabolism
  • Brain Neoplasms* / therapy
  • Disease Progression*
  • Gene Expression Regulation, Neoplastic
  • Glioblastoma* / drug therapy
  • Glioblastoma* / genetics
  • Glioblastoma* / metabolism
  • Glioblastoma* / therapy
  • Humans
  • RNA, Long Noncoding* / genetics
  • RNA, Long Noncoding* / metabolism
  • Signal Transduction*

Substances

  • RNA, Long Noncoding