Nmt1-flox Mouse

Nmt1, short for N-myristoyltransferase 1, is an indispensable eukaryotic enzyme. It catalyzes the transfer of myristoyl groups to the amino-acid terminal residues of numerous proteins. This N-myristoylation process is crucial for the growth and development of many eukaryotes and viruses, and is involved in multiple cellular processes such as signal transduction, cellular transformation, and tumorigenesis [4].

In cancer research, various functional studies have been carried out. In liver cancer, Nmt1 knockdown suppressed tumor growth both in vitro and in vivo. Nmt1-mediated myristoylation of VILIP3 protein promotes liver cancer progression via the NFκB/Bcl-2 signaling pathway [1]. In breast cancer, genetic inhibition of Nmt1 suppressed the initiation, proliferation, and invasion of breast cancer cells in vitro and in vivo. Nmt1 knockdown led to increased oxidative stress and ER stress, activating the JNK pathway and autophagy, which abrogated breast cancer progression, especially in triple-negative breast cancer [3]. In non-small cell lung cancer (NSCLC), Nmt1 enhanced the stemness of NSCLC cells by activating the PI3K/AKT pathway, and was associated with poor survival rates [2]. Also in liver cancer, Nmt1-mediated N-myristoylation was found to be critical. It suppressed anti-tumorigenic proteins and stimulated pro-tumorigenic proteins by interfering with their ubiquitination, resulting in a pro-tumorigenic outcome [5].

In conclusion, Nmt1 is essential for the N-myristoylation of proteins, which is involved in many biological processes. Its role in cancer development has been well-demonstrated through gene knockout (KO) or conditional knockout (CKO) models in various cancer types, including liver, breast, and NSCLC. These findings suggest that targeting Nmt1 could be a potential therapeutic strategy for treating these cancers.