Potential regulation of certain genes at the transcription level for ferroptosis evasion in triple-negative breast cancer (TNBC): A hypothesis       
Yazarlar (1)
Dr. Öğr. Üyesi Çağlar BERKEL Tokat Gaziosmanpaşa Üniversitesi, Türkiye
Makale Türü Diğer (Teknik, not, yorum, vaka takdimi, editöre mektup, özet, kitap krıtiği, araştırma notu, bilirkişi raporu ve benzeri)
Makale Alt Türü SCI, SSCI, AHCI, SCI-Exp dergilerinde yayınlanan teknik not, editöre mektup, tartışma, vaka takdimi ve özet türünden makale
Dergi Adı Medical Hypotheses
Dergi ISSN 0306-9877 Wos Dergi Scopus Dergi
Dergi Tarandığı Indeksler SCI-Expanded
Dergi Grubu Q4
Makale Dili İngilizce
Basım Tarihi 06-2024
Cilt No 189
Sayı 1
DOI Numarası 10.1016/j.mehy.2024.111413
Özet
Ferroptosis is an iron-dependent cell death mechanism, caused by iron accumulation-mediated generation of lipid peroxidation, distinct from other forms of cell death such as pyroptosis [1],[2]. Various mechanisms of ferroptosis evasion exist in tumors. In recent years, many proteins have been identified to influence the vulnerability of breast cancer cells to ferroptotic cell death [3],[4],[5],[6],[7],[8],[9],[10],[11]. Some of these proteins suppress ferroptosis and are associated with ferroptosis resistance/evasion, whereas others promote ferroptosis and increase sensitivity to ferroptotic cell death in breast cancer. Here, those proteins reported in papers published very recently (in 2024) were particularly taken into account. It was found that five proteins which were shown to be associated with ferroptosis inhibition in breast cancer (namely, LAMC2, LPCAT1, POU2F2, SRSF1 and TFAP2C)[3],[4],[5],[6],[7] have higher mRNA ...
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