The Global cancer incidence and mortality data released by the World Health Organization proposes that out of 18.1 million new cancer cases diagnosed, 9.8 million deaths occurred globally in 2018. Cancer is one of the major health burdens among non-communicable diseases globally responsible for impeding life expectancy in the present century. Disrupting hallmarks of cancer (such as prolonged inflammation, increased growth signal, tissue invasion and metastasis, unlimited proliferation and evasion of apoptosis) with dietary agents is of considerable focus for cancer prevention and therapy. In the last decade, a significant contribution has been provided in finding many plant-derived natural agents that can be identified as promising molecular cancer therapeutics. Our focus in this review is on one such natural dietary agent, Morin (3,5,7,2′,4′-pentahydroxyflavone): a bioflavonoid. Morin exerts strong pharmacological properties against a multitude of cancer (liver cancer, cervical cancer, melanoma, breast cancer, prostate, and colon cancer). Recent progress has also been made in examining the potential of morin as a natural dietary agent for fostering the pharmacological effects of other well-known anticancer agents. This review provides an overview of morin and its derivatives in combination with anticancer agents for cancer prevention and therapy.

Background: Aberrant signal transducer and activator of transcription 3 (STAT-3) molecular signaling elicit hepatocellular carcinoma (HCC) in humans. Therefore, targeting STAT-3 is considered as an attractive option towards suppression of HCC in humans. Objective: Our objective is to identify a potential small molecule inhibitor that can specifically target STAT-3 and suppress HCC. Methods: In this study, we analyze a group of sesquiterpene lactone (STL) candidates that has been recently reported in preclinical trials against cancer by a unified computational and experimental approach. Results: Our virtual analysis of the STL candidates revealed Artesunate (ATS) as the best potential inhibitor of STAT-3 with comparable potency to specific inhibitor S3I-201. We also observed that ATS inhibited IL-6 driven STAT-3-DNA binding activity with comparable potency to S3I-201 in a cell free system. Furthermore ATS was observed to interfere with STAT-3 dimerization and suppression of both constitutive and IL-6 inducible STAT-3 in vitro. Nevertheless, we also observed that ATS modulated STAT-3 dependent targets (procaspase-3, Bcl-xl and survivin) favoring occurrence of apoptosis in vitro. Overall, the putative inhibition of STAT-3 by ATS suggested its capacity to interfere with STAT-3 dimerization by binding to the SH2 domain of STAT-3 monomer. It resulted in suppression of STAT-3 and also favored promotion of in vitro cells towards apoptosis. Consequently, ATS also exhibited selective cytotoxicity of cancer cells over normal cells in vitro. Conclusion: All the above observations substantiated by unified computational and in vitro experimental approaches suggested its potential role as a therapeutic anti-cancer agent against HCC.