The tale of SOX2: Focusing on lncRNA regulation in cancer progression and therapy

Life Sci. 2024 May 1:344:122576. doi: 10.1016/j.lfs.2024.122576. Epub 2024 Mar 14.

Abstract

Long non-coding RNAs (lncRNAs) have emerged as influential contributors to diverse cellular processes, which regulate gene function and expression via multiple mechanistic pathways. Therefore, it is essential to exploit the structures and interactions of lncRNAs to comprehend their mechanistic functions within cells. A growing body of evidence has revealed that deregulated lncRNAs are involved in multiple regulations of malignant events including cell proliferation, growth, invasion, and metabolism. SRY-related high mobility group box (SOX)2, a well-recognized member of the SOX family, is commonly overexpressed in various types of cancer, contributing to tumor progression and maintenance of stemness. Emerging studies have shown that lncRNAs interact with SOX2 to remarkably contribute to carcinogenesis and disease states. This review elaborates on the crosstalk between the intricate and complicated functions of lncRNAs and SOX2 in the context of malignant diseases. We elucidate distinct molecular mechanisms that contribute to the onset/advancement of cancer, indicating that lncRNAs/SOX2 axes hold immense promise for potential therapeutic targets. Furthermore, we delve into the modalities of emerging feasible treatment options for targeting lncRNAs, highlighting the limitations of such therapies and providing novel insights into further ameliorations of targeted strategies of lncRNAs to promote the clinical implications. Translating current discoveries into clinical applications could ultimately boost improved survival and prognosis of cancer patients.

Keywords: Cancer progression; Gene therapy; LncRNA; SOX2; Transcription factor.

Publication types

  • Review

MeSH terms

  • Biomarkers, Tumor / genetics
  • Carcinogenesis
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Neoplasms* / drug therapy
  • Neoplasms* / metabolism
  • Neoplasms* / pathology
  • RNA, Long Noncoding* / genetics
  • RNA, Long Noncoding* / metabolism
  • SOXB1 Transcription Factors* / genetics
  • SOXB1 Transcription Factors* / metabolism

Substances

  • Biomarkers, Tumor
  • RNA, Long Noncoding
  • SOX2 protein, human
  • SOXB1 Transcription Factors