RelB-activated GPX4 inhibits ferroptosis and confers tamoxifen resistance in breast cancer

Xu, Zhi; Wang, Xiumei; Sun, Wenbo; Xu, Fan; Kou, Hengyuan; Hu, Weizi; Zhang, Yanyan; Jiang, Qin; Tang, Jinhai; Xu, Yong

doi:10.1016/j.redox.2023.102952

Cited by 8 publications

(3 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, the protein, RelB, provides evidence for the influence of ferroptosis on chemotherapeutic response. RelB promotes resistance to tamoxifen by upregulating GPX4, an enzyme that inhibits ferroptosis ( 169 ). Similarly, miR-155-5p supports the role of pyroptosis in response to therapy.…”

Section: Comparison and Co-action Of Multiple Types Of Rcdmentioning

confidence: 99%

Revolutionizing breast cancer treatment: Harnessing the related mechanisms and drugs for regulated cell death (Review)

Ai,

Yi,

Qiu

et al. 2024

Int J Oncol

View full text Add to dashboard Cite

Breast cancer arises from the malignant transformation of mammary epithelial cells under the influence of various carcinogenic factors, leading to a gradual increase in its prevalence. This disease has become the leading cause of mortality among female malignancies, posing a significant threat to the health of women. The timely identification of breast cancer remains challenging, often resulting in diagnosis at the advanced stages of the disease. Conventional therapeutic approaches, such as surgical excision, chemotherapy and radiotherapy, exhibit limited efficacy in controlling the progression and metastasis of the disease. Regulated cell death (RCD), a process essential for physiological tissue cell renewal, occurs within the body independently of external influences. In the context of cancer, research on RCD primarily focuses on cuproptosis, ferroptosis and pyroptosis. Mounting evidence suggests a marked association between these specific forms of RCD, and the onset and progression of breast cancer. For example, a cuproptosis vector can effectively bind copper ions to induce cuproptosis in breast cancer cells, thereby hindering their proliferation. Additionally, the expression of ferroptosis-related genes can enhance the sensitivity of breast cancer cells to chemotherapy. Likewise, pyroptosis-related proteins not only participate in pyroptosis, but also regulate the tumor microenvironment, ultimately leading to the death of breast cancer cells. The present review discusses the unique regulatory mechanisms of cuproptosis, ferroptosis and pyroptosis in breast cancer, and the mechanisms through which they are affected by conventional cancer drugs. Furthermore, it provides a comprehensive overview of the significance of these forms of RCD in modulating the efficacy of chemotherapy and highlights their shared characteristics. This knowledge may provide novel avenues for both clinical interventions and fundamental research in the context of breast cancer.

show abstract

Section: Comparison and Co-action Of Multiple Types Of Rcdmentioning

confidence: 99%

Revolutionizing breast cancer treatment: Harnessing the related mechanisms and drugs for regulated cell death (Review)

Ai,

Yi,

Qiu

et al. 2024

Int J Oncol

View full text Add to dashboard Cite

show abstract

“…A recent investigation revealed that proferroptotic stimuli, including the inhibition of the lipid hydroperoxidase GPX4 and detachment from the extracellular matrix, result in the upregulation of prominin2, a pentaspanin protein associated with the regulation of lipid dynamics, thereby promoting TNBC [52]. Xu et al reported that elevating GPX4 levels in BC cells leads to an augmentation of tamoxifen (TAM) resistance; conversely, depleting GPX4 in resistant cells decreases TAM resistance [53]. In TNBC cells, miR-324-3p directly targets GPX4.…”

Section: Yap Mediates Resistance To Ferroptosis In Breast Cancermentioning

confidence: 99%

Unleashing the Power of Yes-Associated Protein in Ferroptosis and Drug Resistance in Breast Cancer, with a Special Focus on Therapeutic Strategies

Malla,

Kundrapu,

Bhamidipati

et al. 2023

Cancers

View full text Add to dashboard Cite

The YAP protein is a critical oncogenic mediator within the Hippo signaling pathway and has been implicated in various cancer types. In breast cancer, it frequently becomes activated, thereby contributing to developing drug-resistance mechanisms. Recent studies have underscored the intricate interplay between YAP and ferroptosis within the breast tumor microenvironment. YAP exerts a negative regulatory effect on ferroptosis, promoting cancer cell survival and drug resistance. This review offers a concise summary of the current understanding surrounding the interplay between the YAP pathway, ferroptosis, and drug-resistance mechanisms in both bulk tumor cells and cancer stem cells. We also explore the potential of natural compounds alone or in combination with anticancer therapies for targeting the YAP pathway in treating drug-resistant breast cancer. This approach holds the promise of enhancing the effectiveness of current treatments and paving the way for developing novel therapeutics.

show abstract

“…Induction of cell death by ferroptosis is an emerging anti-cancer strategy with promising pre-clinical outcomes in aggressive, therapy-resistant tumors, some of which even gain ferroptosis susceptibility [ [1] , [2] , [3] , [4] ]. Ferroptosis is distinct from other cell death programs, including apoptosis, necroptosis, pyroptosis, and autophagy, and is driven by excessive membrane peroxidation [ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Iron(III)-salophene catalyzes redox cycles that induce phospholipid peroxidation and deplete cancer cells of ferroptosis-protecting cofactors

Su,

Descher,

Bui-Hoang

et al. 2024

Redox Biology

View full text Add to dashboard Cite

RelB-activated GPX4 inhibits ferroptosis and confers tamoxifen resistance in breast cancer

Cited by 8 publications

References 65 publications

Revolutionizing breast cancer treatment: Harnessing the related mechanisms and drugs for regulated cell death (Review)

Revolutionizing breast cancer treatment: Harnessing the related mechanisms and drugs for regulated cell death (Review)

Unleashing the Power of Yes-Associated Protein in Ferroptosis and Drug Resistance in Breast Cancer, with a Special Focus on Therapeutic Strategies

Iron(III)-salophene catalyzes redox cycles that induce phospholipid peroxidation and deplete cancer cells of ferroptosis-protecting cofactors

Contact Info

Product

Resources

About