Metabolic reprogramming in cancer-associated fibroblasts: a central driver of breast cancer progression

Globally, breast cancer is the most common malignancy in women, with both incidence and mortality rates showing an upward trend. The tumor microenvironment (TME) of breast cancer plays a crucial role in its initiation, progression, and metastasis. Cancer-associated fibroblasts (CAFs), as a key component of the TME, also play a vital role in tumor growth and metastasis. Furthermore, recent studies have found that metabolic reprogramming in CAFs is a key driver of their functional changes, involving significant alterations in CAF metabolic pathways. In addition to meeting their own metabolic demands, CAFs produce nutrients that sustain tumor cell growth. Furthermore, by secreting various cytokines and matrix components, they remodel the tumor microenvironment to promote progression and metastasis, thereby emerging as key drivers of breast cancer malignancy. Current research has elucidated the metabolic characteristics of CAFs in breast cancer, including alterations in glucose, amino acid, and lipid metabolism, and their impact on tumor biology. However, despite numerous studies exploring metabolic reprogramming in CAFs, the underlying specific mechanisms warrant further in-depth investigation. Therefore, this article will delve into CAFs and their metabolic reprogramming mechanisms in breast cancer, as well as their regulatory effects on tumor cells and other immune cells, aiming to provide new potential targets for the clinical treatment of breast cancer.