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Ferroptosis and non-coding RNAs in breast cancer: insights into CAF and TAM interactions

Mohamed J. SaadhFaculty of Pharmacy, Middle East University, Amman, 11831, Jordan. [email protected]Ashok Kumar BishoyiDepartment of Microbiology, Faculty of Science, Marwadi University Research Center, Marwadi University, Rajkot, Gujarat, 360003, IndiaSuhas BallalDepartment of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, IndiaAbhayveer SinghCentre for Research Impact & Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, Punjab, 140401, IndiaAnita DeviDepartment of Chemistry, Chandigarh Engineering College, Chandigarh Group of Colleges-Jhanjeri, Mohali, Punjab, 140307, IndiaGirish Chandra SharmaDepartment of Applied Sciences-Chemistry, NIMS Institute of Engineering & Technology, NIMS University Rajasthan, Jaipur, IndiaAbdusamat ValievDepartment of Anesthesiology and intensive care, pediatric anesthesiology and intensive care, Tashkent Pediatric Medical Institute, Bogishamol Street 223, 100140, Tashkent, UzbekistanK. Satyam NaiduPushpa Negi BhakuniDepartment of Allied Science, Graphic Era Hill University, Bhimtal, IndiaFadhil Faez SeadDepartment of Dentistry, College of Dentistry, The Islamic University, Najaf, Iraq
Discover Oncologyjournal2025en
ABI

Аннотация

Ferroptosis, a form of regulated cell death characterized by the accumulation of lipid peroxides, has emerged as a crucial player in cancer biology, particularly in breast cancer. This review article explores the intricate regulation of ferroptosis by non-coding RNAs (ncRNAs) within the breast cancer tumor microenvironment (TME). We delve into the mechanisms through which various classes of ncRNAs, including microRNAs, long non-coding RNAs, and circular RNAs, modulate the ferroptotic response in breast cancer cells. Furthermore, we examine the interactions between ferroptosis and the TME, specifically focusing on cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs). By highlighting the bidirectional relationships between these components, we aim to elucidate how the modulation of ferroptosis by ncRNAs can influence the behavior of CAFs and TAMs, ultimately impacting tumor progression and therapeutic response. This comprehensive overview underscores the potential of targeting ncRNA-mediated regulation of ferroptosis as a novel therapeutic strategy in breast cancer treatment, with implications for enhancing the efficacy of existing therapies and improving patient outcomes.

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