Therapeutic potential of selenium in breast cancer targeting apoptosis and proliferation pathways

Selenium, an essential trace element, has garnered significant attention for its role in modulating key cellular processes in cancer biology, particularly within breast cancer pathogenesis. Emerging evidence suggests that selenium exhibits a dual role—acting as both an antioxidant and a pro-oxidant—depending on its concentration and chemical form. This dynamic behavior enables selenium to influence critical pathways associated with apoptosis and proliferation, which are often dysregulated in breast cancer. By modulating oxidative stress and redox signaling, selenium plays a unique role in maintaining the balance between cell survival and programmed cell death. Molecular studies have revealed that selenium induces apoptosis in breast cancer cells through both intrinsic and extrinsic pathways, involving mitochondrial dysfunction, caspase activation, and regulation of key genes such as p53, Bax, and Bcl-2. Simultaneously, selenium impairs tumor growth by halting the cell cycle and suppressing proliferative signals via PI3K/Akt/mTOR and MAPK pathways. These anti-proliferative and pro-apoptotic actions position selenium as a promising agent for both prevention and therapy, especially when considered in combination with conventional anticancer drugs. However, selenium’s paradoxical effects at higher doses underscore the need for cautious dose optimization and personalized approaches.