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Ferroptosis is a regulated cell death mechanism distinct from apoptosis, autophagy, and necroptosis, marked by iron accumulation and lipid peroxidation. Since its identification in 2012, it has developed into a potential therapeutic target, especially concerning GI disorders like PC, HCC, GC, and CRC. This interest arises from the distinctive role of ferroptosis in the progression of diseases, presenting a new avenue for treatment where existing therapies fall short. Recent studies emphasize the promise of focusing on ferroptosis to fight GI cancers, showcasing its unique pathophysiological mechanisms compared to other types of cell death. By comprehending how ferroptosis aids in the onset and advancement of GI diseases, scientists aim to discover novel drug targets and treatment approaches. Investigating ferroptosis in gastrointestinal disorders reveals exciting possibilities for novel therapies, potentially revolutionizing cancer treatment and providing renewed hope for individuals affected by these tumors.

The management and treatment of cancer have posed significant challenges in recent years. Conventional chemotherapy, despite its widespread use, has encountered obstacles such as the emergence of drug resistance. As a result, natural products have gained considerable attention as alternative therapies for cancer treatment. These compounds can also be combined with chemotherapy drugs to enhance tumor suppression. Sulforaphane (SFN), a bioactive compound derived from broccoli, has demonstrated remarkable health-promoting properties, including antioxidant, anti-inflammatory, and antidiabetic effects. This review focuses on SFN’s role in cancer treatment, emphasizing its biological mechanisms and ability to regulate drug resistance. Key mechanisms discussed include the regulation of cell death pathways, such as apoptosis, ferroptosis, and autophagy, which are critical in cancer therapy. Additionally, SFN’s ability to suppress metastasis and impair the epithelial-to-mesenchymal transition (EMT) mechanism is highlighted. By inhibiting glycolysis, SFN can reduce the energy supply required for cancer cell proliferation. When combined with chemotherapy drugs, SFN enhances tumor suppression and mitigates drug resistance in human cancers. This is achieved primarily by promoting apoptosis, reducing proliferation, and inhibiting metastasis. In conclusion, SFN shows significant promise in cancer therapy by targeting multiple molecular pathways, improving the efficacy of chemotherapy, and overcoming drug resistance, particularly when incorporated into advanced nanoparticle delivery systems.