Exploring the Key Signaling Pathways and ncRNAs in Colorectal Cancer

Int J Mol Sci. 2024 Apr 21;25(8):4548. doi: 10.3390/ijms25084548.

Abstract

Colorectal cancer (CRC) is the third most prevalent cancer to be diagnosed, and it has a substantial mortality rate. Despite numerous studies being conducted on CRC, it remains a significant health concern. The disease-free survival rates notably decrease as CRC progresses, emphasizing the urgency for effective diagnostic and therapeutic approaches. CRC development is caused by environmental factors, which mostly lead to the disruption of signaling pathways. Among these pathways, the Wingless/Integrated (Wnt) signaling pathway, Phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway, Mitogen-Activated Protein Kinase (MAPK) signaling pathway, Transforming Growth Factor-β (TGF-β) signaling pathway, and p53 signaling pathway are considered to be important. These signaling pathways are also regulated by non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs). They have emerged as crucial regulators of gene expression in CRC by changing their expression levels. The altered expression patterns of these ncRNAs have been implicated in CRC progression and development, suggesting their potential as diagnostic and therapeutic targets. This review provides an overview of the five key signaling pathways and regulation of ncRNAs involved in CRC pathogenesis that are studied to identify promising avenues for diagnosis and treatment strategies.

Keywords: CeRNA; MAPK signaling pathway; PI3K/AKT/mTOR signaling pathway; TGF-β signaling pathway; Wnt signaling pathway; circular RNA; colorectal cancer; long non-coding RNA; miRNA; p53 signaling pathway.

Publication types

  • Review

MeSH terms

  • Animals
  • Colorectal Neoplasms* / genetics
  • Colorectal Neoplasms* / metabolism
  • Colorectal Neoplasms* / pathology
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • MicroRNAs / genetics
  • MicroRNAs / metabolism
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism
  • RNA, Untranslated* / genetics
  • RNA, Untranslated* / metabolism
  • Signal Transduction*

Substances

  • RNA, Untranslated
  • MicroRNAs
  • RNA, Long Noncoding

Grants and funding

This research received no external funding.