Unveiling the connection: Long-chain non-coding RNAs and critical signaling pathways in breast cancer

Pathol Res Pract. 2023 Sep:249:154736. doi: 10.1016/j.prp.2023.154736. Epub 2023 Aug 3.

Abstract

Breast cancer is a complex and diverse condition that disrupts multiple signaling pathways essential for cell proliferation, survival, and differentiation. Recently, the significant involvement of long-chain non-coding RNAs (lncRNAs) in controlling key signaling pathways associated with breast cancer development has been discovered. This review aims to explore the interaction between lncRNAs and various pathways, including the AKT/PI3K/mTOR, Wnt/β-catenin, Notch, DNA damage response, TGF-β, Hedgehog, and NF-κB signaling pathways, to gain a comprehensive understanding of their roles in breast cancer. The AKT/PI3K/mTOR pathway regulates cell growth, survival, and metabolic function. Recent data suggests that specific lncRNAs can influence the functioning of this pathway, acting as either oncogenes or tumor suppressors. Dysregulation of this pathway is commonly observed in breast cancer cases. Moreover, breast cancer development has been associated with other pathways such as Wnt/β-catenin, Notch, TGF-β, Hedgehog, and NF-κB. Emerging studies have identified lncRNAs that modulate breast cancer's growth, progression, and metastasis by interacting with these pathways. To advance the development of innovative diagnostic tools and targeted treatment options, it is crucial to comprehend the intricate relationship between lncRNAs and vital signaling pathways in breast cancer. By fully harnessing the therapeutic potential of lncRNAs, there is a possibility of developing more effective and personalized therapy choices for breast cancer patients. Further investigation is necessary to comprehensively understand the role of lncRNAs within breast cancer signaling pathways and fully exploit their therapeutic potential.

Keywords: Breast cancer; LncRNA; NF-κB; Notch; TGF-β; Wnt/β-catenin.

Publication types

  • Review

MeSH terms

  • Animals
  • Breast Neoplasms* / genetics
  • Female
  • Gene Expression Regulation, Neoplastic / genetics
  • Hedgehogs / genetics
  • Hedgehogs / metabolism
  • Humans
  • NF-kappa B / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA, Long Noncoding* / genetics
  • RNA, Long Noncoding* / metabolism
  • Signal Transduction
  • TOR Serine-Threonine Kinases / metabolism
  • Transforming Growth Factor beta / metabolism
  • beta Catenin / metabolism

Substances

  • RNA, Long Noncoding
  • beta Catenin
  • Proto-Oncogene Proteins c-akt
  • NF-kappa B
  • TOR Serine-Threonine Kinases
  • Transforming Growth Factor beta
  • Phosphatidylinositol 3-Kinases