Molecular mechanisms and pathophysiological implications of mucin-type O-glycosylation dysregulation in colorectal cancer progression.

Colorectal cancer (CRC) is among the most prevalent malignancies globally, with 1.9 million new cases annually. While CRC pathogenesis has been widely attributed to the adenoma-carcinoma and serrated sequences, our study highlights the critical and multifaceted role of O-glycosylation impairment in this malignancy. Mucin-type O-glycosylation, a key post-translational modification, exerts significant effects on tumor cells, impacting their proliferation, migration, and invasiveness. Additionally, its influence on the immune response to CRC presents novel perspectives for potential therapeutic interventions. The authors conducted a systematic literature review following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, using databases such as Google Scholar, PubMed, and Scopus. In this article, we provide a comprehensive analysis of the mechanisms underlying mucin-type O-glycosylation disruption in CRC and examine how these mechanisms could serve as biomarkers for early diagnosis and personalized treatment strategies. Our findings contribute to a more detailed understanding of CRC pathogenesis and offer promising directions for innovative diagnostic and therapeutic approaches, which in the future may lead to improved patient prognosis.