CAF-derived GLUT1 and its role in modulating ovarian cancer progression: a multi-dimensional analysis of the tumor microenvironment.

Deciphering the reprogramming of glucose metabolism in cancer-associated fibroblasts (CAFs) within the ovarian cancer (OC) microenvironment is essential for understanding tumor progression. While CAFs are known to influence tumor metabolism, the specific mechanisms underlying their role in metabolic adaptation remain unclear. Here, we show that GLUT1 is highly expressed in CAFs and promotes glucose uptake, glycolysis, and lactate production, which in turn drives OC cell proliferation and migration via the TGF-β1/p38/MMP2/MMP9 pathway. Single-cell RNA sequencing and bioinformatics analyses identify GLUT1 as a key metabolic regulator in CAFs, and 3D bioprinting models further confirm its role in shaping the tumor microenvironment. These findings highlight GLUT1 as a potential therapeutic target for OC and provide new insights into tumor metabolism and metastasis.