Breast cancer (BC) refers to a malignant neoplasm that takes place in the epithelial tissue of the breast. α-Cyperone (α-CYP) is one of the principal active components of Cyperus rotundus . However, research on the role of α-CYP in the development of BC is still lacking. This study investigates the effect and underlying mechanism of α-CYP in the progression of BC. Our findings revealed that both low-dose and high-dose α-CYP inhibited the colony formation ability of MCF-7 and BT474 cells, accompanied by the decrease in Ki67 expression and the obstruction of the cell cycle. Moreover, α-CYP treatment increased the activity of caspase-3, which leads to an increase in apoptosis. Moreover, the combination of α-CYP and cisplatin (DDP) remarkably suppressed cell viability and further facilitated apoptosis, indicating that α-CYP could enhance the sensitivity of chemotherapeutic agents in BC cells. Further, α-CYP treatment decreased TRIM24 expression through the ubiquitin–proteasome pathway. Notably, α-CYP counteracted the robust proliferation of BC cells triggered by TRIM24 overexpression. Taken together, this study confirmed that α-CYP is an effective anticancer component for BC treatment. α-CYP inhibits proliferation and induces apoptosis of BC cells via the modulation of TRIM24.
Yttrium oxide nanoparticles (Y 2 O 3 NPs), extensively utilized rare earth nanoparticles, exhibited a diverse range of applications across various fields, which leading to increased human exposure. Moreover, potential neurotoxic risks have been associated with their use, yet the underlying mechanism remains unclear. The present study aimed to investigate the effects of Y 2 O 3 NPs on cognitive function in rats with a particular focus on elucidating the pivotal role played by astrocytes in this process. The results demonstrated that Y 2 O 3 NPs induced cognitive and memory impairment in rats, copper (Cu) accumulation and cuproptosis of astrocytes as contributing factors. Furthermore, we elucidated that Y 2 O 3 NPs induced astrocytes cuproptosis by inhibiting TRIM24/DTNBP1/ATP7A signaling pathway-mediated cellular Cu efflux. We provide, for the first time, the important involvement of astrocytes in Y 2 O 3 NPs-induced neurotoxicity, elucidating that cuproptosis as the primary mode of cell death. These results offer valuable insights for the future safe application of rare earth nanoparticles in field of neurology.
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