Decoding aberrant glycosylation in colorectal cancer: From Glycosyaltion characterization, expression regulation to

Zihan Li1, Xichen Dong1, Jian Liu1

  • 1Medical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.

Insights

Colorectal cancer (CRC) involves significant changes in glycosylation, impacting tumor growth and the tumor microenvironment (TME). Understanding these CRC glycosylation alterations is key for developing new diagnostic and therapeutic strategies.

Area of Science:

  • Biochemistry
  • Oncology
  • Molecular Biology

Background:

  • Colorectal cancer (CRC) displays widespread changes in glycosylation, affecting glycan structures, terminal modifications, and enzyme activity.
  • These glycosylation alterations are linked to malignant behaviors like invasion, migration, proliferation, and the creation of an immunosuppressive tumor microenvironment (TME).

Purpose of the Study:

  • To review major glycosylation types in CRC, including O-GalNAc glycosylation, O-GlcNAcylation, N-glycosylation, sialylation, glycosphingolipids, and glycosaminoglycans.
  • To explore how glycosylation reprogramming influences oncogenic signaling and cellular plasticity in CRC.
  • To highlight advancements in CRC-specific glycosylation-based diagnostics, prognostics, and therapeutics.

Main Methods:

  • Literature review of glycosylation alterations in colorectal cancer.
  • Summary of key enzymes involved in glycosylation biosynthesis.
  • Analysis of the role of glycosylation in oncogenic signaling and TME modulation.
  • Review of current diagnostic, prognostic, and therapeutic strategies targeting CRC glycosylation.

Main Results:

  • Detailed delineation of various glycosylation types implicated in CRC.
  • Explanation of the enzymatic machinery governing CRC glycosylation.
  • Exploration of the link between glycosylation reprogramming, oncogenic signaling, and cellular plasticity.
  • Identification of recent progress in CRC-specific glycosylation-based strategies.

Conclusions:

  • Glycosylation alterations are central to CRC pathogenesis and TME.
  • Understanding CRC glycosylation provides a framework for improved diagnostics and therapeutics.
  • Targeting CRC-specific glycosylation holds promise for enhanced early diagnosis, prognostic assessment, and treatment strategies.