Pharmacological Properties to Pharmacological Insight of Sesamin in Breast Cancer Treatment: A Literature-Based Review Study

Figure 2

Graphical presentation of the molecular pharmacology of sesamin in breast cancer. Sesamin and its metabolites have potential antibreast cancer activities. In the early stage, the mechanism is mediated through regulation of extracellular receptor-like estrogen receptor-α (ER-α), estrogen receptor-β (ER-β), programmed death-ligand 1 (PD-L1), Herceptin epidermal growth receptor 2 (HER-2), and epidermal growth factor receptor (EGFR). Through this receptor, sesamin and its metabolites inhibit some major signaling molecules like pAkt-PI3K/mTOR and JAK/STAT. These tumor intrinsic signals upregulate activator protein 1 (AP-1), inhibit estrogen-responsive elements (ERE), and activate other regulatory proteins. Sesamin and metabolites finally inhibit cell cycle progression by the suppression of cyclin and its associated enzyme kinase (CKD 2, 4, and 6); inhibit metastasis and angiogenesis by the suppression of MMP 2, MMP 9, ICAM-1, and VEGF; and induce apoptosis by the upregulation of Bax, caspase 3, P²¹, and P⁵³ with downregulation of Bcl2 and survivin protein.