Fads2, also known as acyl-CoA 6-desaturase, is a key enzyme in long-chain polyunsaturated fatty acid (LC-PUFA) biosynthesis [5]. It is involved in the desaturation of fatty acids, catalyzing biosynthesis of several unsaturated fatty acids by Δ6, Δ8, and Δ4 desaturation, and is thus crucial for fatty acid metabolism pathways [1]. Fads2's activity has significant implications for various biological processes, and genetic models can be valuable for studying its functions.

Fads2 silencing in MCF7 cells and in vivo breast cancer models causes the synthesis of sciadonic acid, which lacks the internal Δ8 double bond required for the synthesis of prostaglandin and leukotriene, among other eicosanoids [1]. In ascites-derived ovarian cancer cells, genetic ablation of FADS2 retarded tumor growth, cancer stem cell formation, and reduced platinum resistance [2]. In cholangiocarcinoma, FADS2 depletion reduced in vivo tumorigenicity, cell proliferation, migration, and sphere-forming ability, and increased apoptotic cell death and ferroptosis markers [4]. In mouse embryonic fibroblasts, inhibiting mTOR signaling, which is related to FADS2 expression, decreased FADS2 expression and sapienate biosynthesis [3].

In conclusion, Fads2 plays a vital role in fatty acid metabolism. Through gene-knockout and related models, its impact on cancer development and progression has been revealed, such as in breast, ovarian, and cholangiocarcinoma. These studies help us understand the role of Fads2 in disease-related biological processes and may provide potential targets for cancer treatment [1,2,3,4].