Nfya, also known as Nuclear Factor-Y Subunit A, is a transcription factor that plays crucial roles in multiple biological processes. It is involved in pathways related to cell metabolism, proliferation, and development. The NF-Y protein complex, of which Nfya is a part, regulates the transcription of numerous genes, especially those functioning in the G1/S cell cycle transition [3].

In mouse fetal heart development, loss of Nfya leads to altered cardiomyocyte composition, reduced proliferation, and impaired mitochondrial metabolism, resulting in cardiac growth defects and embryonic death. Nfya, interacting with cofactor SP2, activates genes linking metabolism and proliferation at the transcription level, highlighting its nodal role in prenatal cardiac growth and heart metabolism regulation [1]. In castration-resistant prostate cancer (CRPC), silencing Nfya in androgen-independent cell lines impedes cell growth and migration. RNA-seq analysis identifies EGR4 as a downstream target of Nfya, and in vivo studies in a mouse model show that Nfya silencing inhibits xenograft tumor growth [2].

In conclusion, Nfya is essential for normal development, as demonstrated by its role in mouse heart development. Its study through gene knockout (KO) or conditional knockout (CKO) mouse models has revealed its significance in diseases such as CRPC. Understanding Nfya's functions provides insights into the underlying mechanisms of development and disease, which may help in developing therapeutic strategies for related conditions.