Chapter 12 - Role of Emodin in Chemosensitization of Cancer

Abstract

Because of safety, affordability, ready availability, and limited toxicity, agents derived from Mother Nature possess a potential for the prevention and treatment of cancer. Emodin (EM), an anthraquinone derived from shrubs, herbs, flowering plants, and spices, is one such agent that exhibits activities against hepatocellular carcinoma, pancreatic cancer, breast cancer, non-small-cell lung cancer, ovarian cancer, and prostate cancer. The anthraquinone can sensitize resistant tumor cells to chemotherapeutic agents such as TNF-related apoptosis-inducing ligand (TRAIL), oxaliplatin, gemcitabine, adriamycin, cisplatin, capecitabine, paclitaxel, abiplastin, doxorubicin, and 5-fluorouracil. The anthraquinone can modulate multiple cancer-related cell signaling pathways such as AKT8 virus oncogene cellular homologue (AKT), extracellular signal-regulated kinase (ERK)1/2, Janus-associated kinase (JAK)2, C-X-C chemokine receptor type 4 (CXCR4), signal transducers and activators of transcription 3 (STAT3), nuclear factor kappa B (NF-κB), activator protein-1 (AP-1), cyclooxygenase-2 (COX-2), and many other pathways. The modulation of these cell signaling pathways by the anthraquinone might contribute to its anticancer and chemosensitization activities. The anticancer properties of EM have been reported both by in vitro and rodent studies. However, EM has still not been tested in humans for its anticancer activities. The focus of this chapter is to discuss the anticancer and chemosensitizing activities of EM. The underlying mechanisms for EM anticancer activities are discussed.