Emodin Inhibits Inflammation, Carcinogenesis, and Cancer Progression in the AOM/DSS Model of Colitis-Associated...

Area of Science:

• Oncology
• Gastroenterology
• Pharmacology

Background:

• Colorectal cancer (CRC) is a major global health concern.
• Chronic inflammation is a key driver in CRC development and progression.
• Emodin, a natural anthraquinone, exhibits antioxidant, anti-inflammatory, and anti-tumor properties.

Purpose of the Study:

• To investigate the effects of Emodin on inflammation and tumorigenesis in the AOM/DSS model of colitis-associated CRC.
• To evaluate Emodin's impact on inflammatory markers, immune cell infiltration, and tumor progression.
• To assess Emodin's efficacy in both in vivo and in vitro models of CRC.

Main Methods:

• Utilized the azoxymethane (AOM)/dextran sodium sulfate (DSS) mouse model for colitis-associated intestinal tumorigenesis.
• Administered Emodin (50 mg/kg) and assessed inflammation, immune cell markers (CD11b, F4/80, CD3), cytokine profiles (TNFα, IL1α/β, IL6, CCL2, CXCL5), and enzyme expression (COX-2, NOS2) at 3, 5, and 14 weeks.
• Evaluated tumor incidence, size, invasiveness, and clinical symptoms (bleeding, diarrhea).
• Conducted in vitro studies using LPS-stimulated RAW 264.7 macrophages and colon cancer cell lines (SW620, HCT116) to assess Emodin's effects on inflammatory mediators, cell viability, adhesion, migration, and invasion.

Main Results:

• Emodin significantly reduced inflammatory cell recruitment and pro-inflammatory mediator expression in the tumor microenvironment at all time points.
• Emodin suppressed the incidence and progression of premalignant and malignant lesions, including adenomas, dysplastic lesions, and carcinomas.
• Emodin alleviated acute intestinal symptoms and, in vitro, inhibited inflammatory responses and reduced colon cancer cell viability, adhesion, migration, and invasion.

Conclusions:

• Emodin effectively suppresses inflammation associated with colorectal cancer development.
• Emodin demonstrates preventative effects against AOM/DSS-induced intestinal tumorigenesis and progression.
• These findings suggest Emodin holds potential as a natural agent for CRC prevention and treatment.