Exploring Tephrosin: A review of its potential in cancer therapy and multifaceted anticancer mechanisms

Abstract

Cancer statistics highlight diverse susceptibilities, necessitating tailored global research and interventions. Conventional cancer treatments like chemotherapy and radiotherapy lack specificity, causing severe side effects. Novel targeted therapies exert cytostatic effects by modulating cell cycle regulators, disrupting microtubules, or inducing apoptosis. Tephrosin, a rotenoid isoflavonoid found in the family Fabaceae, exhibits promising anticancer properties against various cancer types. This review aimed to comprehensively summarize tephrosin's anticancer activity, explore its mode of action and safety profile, and address gaps in the literature regarding its pharmacokinetics and pharmacodynamics. Tephrosin exerted anticancer activities against skin, cervical, breast, ovarian, pancreatic, colorectal, lung, and leukemia. Tephrosin acts through various pathways including inhibiting NF-κB signaling, inhibiting autophagy, inducing different types of apoptosis, inhibiting elongation factor-2 kinase, reducing the phosphorylation of growth factors, blocking downstream signaling pathways such as PI3K/Akt and Ras/MAPK, p38/MAPK, and STAT3, arresting the cell cycle at the G2/M phase, inducing DNA damage and oxidative stress in cancer cells, and suppression of enzymes involved in extracellular matrix degradation and metastasis. This review revealed the lack of antioxidant, pharmacodynamics, and pharmacokinetics studies on this promising isoflavonoid. Tephrosin's multifaceted mechanisms make it a compelling candidate for further investigation in cancer therapy.