ΔA146Ply exerts anti-triple-negative breast cancer effects by inducing ferroptosis via regulation of the CYP24A1-mediated calcitriol-vitamin D receptor pathway.

Authors

Ye Yu, Zhengkun Zhang, Dingxue Wang, Xin Bai, Dan He, Xuxu Ji, Zhaoru Yin, Keyi Xu, Ji Liu, Jiaqiong Zou

Published in

Toxicology and applied pharmacology. Pages 118025. Aug 30, 2026. Epub Aug 30, 2026.

Abstract

Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype, typically associated with poor clinical outcomes. Recently, ferroptosis has emerged as a promising therapeutic target for TNBC. ΔA146Ply, a novel pneumolysin variant, has demonstrated potential as an anti-tumor agent; however, its role in regulating ferroptosis remains unclear. This study investigates whether ΔA146Ply exerts anti-TNBC effects by promoting ferroptosis via the CYP24A1-mediated Calcitriol/vitamin D receptor (VDR) pathway. Our in vitro results reveal that ΔA146Ply inhibits MDA-MB-231 cells by inducing ferroptosis. Mechanistically, we demonstrate that CYP24A1 negatively regulates the Calcitriol-VDR pathway and serves as a critical mediator of ferroptosis. In vivo, ΔA146Ply suppresses TNBC tumor growth by downregulating CYP24A1 and promoting ferroptosis. In conclusion, ΔA146Ply exerts anti-TNBC effects by activating ferroptosis through the regulation of the CYP24A1-mediated Calcitriol-VDR pathway.

PMID:
42669384
Bibliographic data and abstract were imported from PubMed on 31 Aug 2026.

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