FSTL3 overexpressed is key factor modulating the ovarian tumor microenvironment of syngenic mouse model

This study aims to investigate the role of FSTL3 in ovarian cancer progression and treatment resistance in HGSOC, and validate FSTL3 as a potential therapeutic target. We found that FSTL3 expression was associated with a fibrotic microenvironment, correlating with an increased abundance of cancer-associated fibroblasts (CAFs), cancer cells with a more mesenchymal phenotype. Tumors overexpressing FSTL3 revealed immune evasion, notably by reducing immunocytes infiltration. Overall design: To investigate the role of FST and FSTL3 in modulating the tumor microenvironment, we engineered cancer cell models by knocking out FST (FSTKO) and overexpressing human FSTL3 in our KPCA syngeneic ovarian cancer cells. These modified cells were then intraperitoneally grafted into C57BL/6 mice. Tumors were harvested and dissociated for single cell RNA library constuction and sequencing (N=4 pooled tumors per genotype, 5 000 cells)