Samd4b, also known as Smaug2, is a member of the SAMD4 protein family, which are novel RNA-binding proteins. It contains a sterile alpha motif (SAM) domain, and can mediate post-transcriptional regulation and translation repression in eukaryotes. SAMD4 proteins, including Samd4b, can bind to target mRNAs through stem-loop structures (Smaug recognition elements, SREs) to regulate mRNA stability, degradation and translation [3].

In hepatocellular carcinoma (HCC), a tumor suppressor gene SAMD4B was found to be involved in a synergistic immunochemotherapy strategy. Reduced mutations of upstream genes NOTCH1 and NOTCH2 increased SAMD4B, which affected the instability of APOA2 mRNA by 2'-O-Methylation modification of the C-terminus. The decreased APOA2 further attenuated programmed death ligand 1 (PD-L1) level, improving the immune microenvironment and achieving an antitumor effect [1].

In colorectal cancer, miR-451 was shown to suppress the malignant characteristics of the cancer via targeting SAMD4B. Overexpression of miR-451 inhibited proliferation and migration, promoted apoptosis and enhanced the sensitivity of CRC cells to chemotherapy [2].

In conclusion, Samd4b plays a significant role in post-transcriptional regulation. Its dysregulation is associated with cancer development, as demonstrated in hepatocellular carcinoma and colorectal cancer models. Understanding Samd4b's function provides potential therapeutic targets for these diseases, highlighting the importance of studying Samd4b in the context of disease mechanisms.