Ferroptosis as a promising targeted therapy for triple negative breast cancer

Mokhtarpour, Kasra; Razi, Sepideh; Rezaei, Nima

doi:10.1007/s10549-024-07387-7

Breast Cancer Res Treat

2024

DOI: 10.1007/s10549-024-07387-7

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Ferroptosis as a promising targeted therapy for triple negative breast cancer

Kasra Mokhtarpour,

Sepideh Razi,

Nima Rezaei

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2024

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Cited by 2 publications

References 165 publications

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TFAP2A Promotes Cell Progression and Suppresses Ferroptosis in Lung Adenocarcinoma via Activating Transcription of CST1

Luan,

Peng,

Hui

et al. 2024

J Biochem & Molecular Tox

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Lung adenocarcinoma (LUAD) is a common type of lung cancer with complicated pathological mechanism. Transcription Factor AP‐2 Alpha (TFAP2A) and Cysteine protease inhibitor 1 (CST1) are upregulated genes in LUAD samples, accordingly, we focused on clarifying the role of TFAP2A/CST1 axis in LUAD. Expression analysis was performed using real‐time quantitative polymerase chain reaction and western blot. Cellular behaviors were detected by colony formation assay, EdU assay, wound healing assay and flow cytometry. Ferroptosis was assessed by oxidative indicators, Fe2+ level and related proteins. TFAP2A and CST1 interaction was analyzed via ChIP assay and dual‐luciferase reporter assay. TFAP2A function in vivo was evaluated by xenograft tumor assay. CST1 was overexpressed in LUAD samples and cells. Downregulation of CST1 inhibited proliferation, migration but it promoted apoptosis and ferroptosis of LUAD cells. TFAP2A interacted with the promoter of CST1 to up‐regulate CST1 expression. TFAP2A regulated the malignant behaviors and ferroptosis of LUAD cells by targeting CST1. TFAP2A affected LUAD tumor growth via mediating CST1. All these data proved that TFAP2A/CST1 axis contributed to proliferation, migration while it suppressed apoptosis and ferroptosis in LUAD.

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TFAP2A Promotes Cell Progression and Suppresses Ferroptosis in Lung Adenocarcinoma via Activating Transcription of CST1

Luan,

Peng,

Hui

et al. 2024

J Biochem & Molecular Tox

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Targeting ferroptosis: a promising strategy to overcome drug resistance in breast cancer

Peng,

Chen,

Jiang

2024

Front. Oncol.

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Breast cancer is one of the most prevalent malignancies affecting women worldwide, with its incidence increasingly observed in younger populations. In recent years, drug resistance has emerged as a significant challenge in the treatment of breast cancer, making it a central focus of contemporary research aimed at identifying strategies to overcome this issue. Growing evidence indicates that inducing ferroptosis through various mechanisms, particularly by inhibiting System Xc-, depleting glutathione (GSH), and inactivating glutathione peroxidase 4 (GPX4), holds great potential in overcoming drug resistance in breast cancer. It is anticipated that therapies targeting ferroptosis will emerge as a promising strategy to reverse tumor resistance, offering new hope for breast cancer patients. This review will explore the latest advancements in understanding ferroptosis in the context of breast cancer drug resistance, with a particular emphasis on the roles of ferroptosis inducers and inhibitors, and the impact of ferroptotic pathways on overcoming drug resistance in breast cancer.

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Ferroptosis as a promising targeted therapy for triple negative breast cancer

Cited by 2 publications

References 165 publications

TFAP2A Promotes Cell Progression and Suppresses Ferroptosis in Lung Adenocarcinoma via Activating Transcription of CST1

TFAP2A Promotes Cell Progression and Suppresses Ferroptosis in Lung Adenocarcinoma via Activating Transcription of CST1

Targeting ferroptosis: a promising strategy to overcome drug resistance in breast cancer

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