SOD1-high fibroblasts derived exosomal miR-3960 promotes cisplatin resistance in triple-negative breast cancer by suppressing BRSK2-mediated phosphorylation of PIMREG

Platinum-based neoadjuvant therapy represented by cisplatin is widely employed in treating Triple-Negative Breast Cancer (TNBC), a particularly aggressive subtype of breast cancer. Nevertheless, the emergence of cisplatin resistance presents a formidable challenge to clinical chemotherapy efficacy....

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Veröffentlicht in:	Cancer letters 2024-05, Vol.590, p.216842-216842, Article 216842
Hauptverfasser:	Li, Kangdi, Lin, Han, Liu, Anyi, Qiu, Cheng, Rao, Zejun, Wang, Zhihong, Chen, Siqi, She, Xiaowei, Zhu, Shengyu, Li, Pengcheng, Liu, Lang, Wu, Qi, Wang, Guihua, Xu, Feng, Li, Shaotang
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antineoplastic Agents - pharmacology BRSK2 Cell Line, Tumor Cisplatin - pharmacology Drug Resistance, Neoplasm Exosomes Exosomes - genetics Exosomes - metabolism Female Fibroblasts Fibroblasts - drug effects Fibroblasts - metabolism Gene Expression Regulation, Neoplastic - drug effects Humans Mice MicroRNAs - genetics MicroRNAs - metabolism miR-3960 NF-kappa B - genetics NF-kappa B - metabolism Phosphorylation Signal Transduction - drug effects Superoxide Dismutase-1 - genetics Superoxide Dismutase-1 - metabolism Triple Negative Breast Neoplasms - drug therapy Triple Negative Breast Neoplasms - genetics Triple Negative Breast Neoplasms - metabolism Triple Negative Breast Neoplasms - pathology Triple-negative breast cancer Tumor Microenvironment
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