Bediwi Alaa Khalaf, Hjazi Ahmed, Kedhem Mundher, Alkhathami Ali G, S RenukaJyothi, Nayak Priya Priyadarshini, Pargaien Amrita, Singh Udaybir, Hammady Fathi Jihad, Salih Salah Abdulhadi
Medical Laboratory Techniques Department, College of Health and Medical Technology, University of Al-Maarif, Anbar, Ramadi, Iraq.
Department of Medical Laboratory, College of Applied Medical Sciences, Prince Sattam Bin Abdulaziz University, 11942, Al-Kharj, Saudi Arabia.
Naunyn Schmiedebergs Arch Pharmacol. 2025 Jul 1. doi: 10.1007/s00210-025-04390-7.
Breast cancer (BC) cells are distinguished by their capacity to reconfigure metabolism to support rapid growth and survive in hypoxic, nutrient-deficient environments. In the breast tumor microenvironment (TME), metabolic changes-including the Warburg effect, modifications in Krebs cycle intermediates, and adjusted oxidative phosphorylation-are closely associated with the dynamic signaling between tumor cells and stromal elements. Cancer-associated fibroblasts (CAFs), a diverse and adaptable group inside the stroma, significantly influence metabolic pathways, including those regulating glucose, amino acid, and lipid metabolism. Recent research underscores that the metabolic interaction between BC cells and CAFs not only promotes tumor growth and invasion but also facilitates treatment resistance. This review is aimed at consolidating the existing data on the metabolic interactions between BC cells and CAFs, highlighting molecular mechanisms and pathways that could represent potential targets for future therapies.
乳腺癌（BC）细胞的特点是能够重新配置新陈代谢，以支持快速生长并在缺氧、营养缺乏的环境中存活。在乳腺肿瘤微环境（TME）中，代谢变化——包括瓦伯格效应、三羧酸循环中间体的改变以及氧化磷酸化的调整——与肿瘤细胞和基质成分之间的动态信号传导密切相关。癌症相关成纤维细胞（CAFs）是基质内一个多样且适应性强的群体，对代谢途径有显著影响，包括那些调节葡萄糖、氨基酸和脂质代谢的途径。最近的研究强调，BC细胞与CAFs之间的代谢相互作用不仅促进肿瘤生长和侵袭，还会导致治疗耐药性。本综述旨在整合关于BC细胞与CAFs之间代谢相互作用的现有数据，突出那些可能成为未来治疗潜在靶点的分子机制和途径。
