Research demonstrates that diselenide compounds impair Akt/mTOR and ERK signaling in triple-negative breast cancer, suggesting a novel therapeutic approach.
Organochalcogens exhibit promising chemotherapeutic potential against several cancer types. However, their ability to simultaneously target interconnected oncogenic signaling networks remains mostly unexplored. Herein, we report 4-nitro-substituted benzylic diselenide 7, which exhibits concerted inhibition of Akt/mTOR and ERK pathways with the suppression of NF-κB-mediated inflammation and invasiveness against the highly aggressive triple-negative breast cancer MDA-MB-231 cells. Detailed mechanistic investigations illustrated that diselenide 7 induces ROS, leading to DNA damage, mitochondrial dysfunction, and consequent suppression of the Akt/mTOR-ERK1/2 signaling axis, leading to cellular death. Furthermore, the potency of 7 was validated in Swiss albino mice bearing breast adenocarcinoma, with a markedly reduced tumor volume, downregulation of VEGF/MMP-9 expressions indicating impaired angiogenesis/metastasis, and the expansion of life span. This work exemplifies distinctive mechanistic insights into the multitargeting agent diselenide 7, highlighting its potential as an anticancer therapeutic and paving the way for the development of small-molecule organoselenium compounds for the effective treatment of cancer.
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Barman et al. (2025) studied this question.
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