Therapeutic Role of Morin in Colorectal Cancer: Molecular Mechanisms

Abstract

Colorectal cancer (CRC), the third most prevalent cancer in the world, typically originates from abnormal crypts in the intestine generated by cancer stem cells (CSCs). Subsequently, these abnormal crypts progressively evolve into polyps and eventually colorectal cancer through multiple molecular mechanisms. During carcinogenesis and progression, morin, a flavonoid with diverse pharmacological activities, exhibits remarkable anti-cancer effects. Numerous studies have confirmed that morin exerts inhibitory effects on CRC through multiple pathways, including the regulation of reactive oxygen species (ROS) levels, suppression of nuclear factor κ-B (NF-κB) activity, induction of apoptosis, inhibition of tumor energy metabolism, and suppression of CSCs. The anti-cancer effects of morin involve several signaling pathways, such as PRKR-like endoplasmic reticulum kinase (PERK)/Nuclear factor erythroid 2-related factor 2 (Nrf2), NF-κB, AKT, β-cateinin/c-Myc, and signal transducer and activator of transcription 3 (STAT3). Furthermore, combination therapy involving morin with other anti-cancer drugs enhances sensitivity to 5-fluorouracil, thereby exerting an effect on drug-resistant colorectal cancer. This paper reviews the pharmacokinetic properties of morin, along with its anticancer effects and underlying mechanisms in CRC. Given its multi-targeted pharmacological effects, capacity to enhance the efficacy of other anti-cancer medications, and excellent safety profile, morin exhibits promising potential as a preventive and therapeutic intervention for CRC.