Defensins: Exploring Their Opposing Roles in Colorectal Cancer Progression

• Published in: Cancers Vol. 16; no. 15; p. 2622
• Main Authors: Sabit, Hussein, Pawlik, Timothy M, Abdel-Ghany, Shaimaa, Arneth, Borros
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.08.2024
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Antimicrobial activity; Apoptosis; Cancer; Cancer therapies; Cell cycle; Cell death; Cell growth; Cell proliferation; Cell survival; Clinical outcomes; colon cancer; Colorectal cancer; Colorectal carcinoma; CRC; Defensins; Disease; Drug resistance; Gene expression; Growth factors; Growth regulators; gut microbiota; Health aspects; Intestinal microflora; Kinases; Medical prognosis; Metabolism; Metastasis; Microbiomes; Molecular modelling; Mortality; mTOR; Patients; Physiological aspects; Protein synthesis; Proteins; TOR protein; Tumorigenesis; Vincristine; mTOR; defensins; colorectal cancer; CRC; colon cancer; gut microbiota
• ISSN: 2072-6694; 2072-6694
• DOI: 10.3390/cancers16152622

Colorectal cancer (CRC) represents a significant global healthcare burden, with a particularly concerning rising incidence among younger adults. This trend may highlight potential links between diet, gut microbiome, and CRC risk. Novel therapeutic options have been increasingly based on the understanding of molecular mechanisms and pathways. The PI3K/AKT/mTOR pathway, a crucial cell growth regulator, offers a promising target for CRC therapy. mTOR, a key component within this pathway, controls cell growth, survival, and metabolism. Understanding the specific roles of defensins, particularly human β-Defensin 1 (HBD-1), in CRC is crucial. HBD-1 exhibits potent antimicrobial activity and may influence CRC development. Deciphering defensin expression patterns in CRC holds the promise of improved understanding of tumorigenesis, which may pave the way for improved diagnostics and therapies. This article reviews recent advances in understanding regarding how HBD-1 influences CRC initiation and progression, highlighting the molecular mechanisms by which it impacts CRC. Further, we describe the interaction between defensins and mTOR pathway in CRC.