Rps16, ribosomal protein S16, is a crucial component of the ribosome, playing a vital role in translation initiation. It is involved in the assembly of ribosomal subunits and the formation of functional preinitiation complexes, thus being essential for protein synthesis. It has been associated with various biological processes and diseases [2].

In hepatocellular carcinoma (HCC), the USP1-RPS16 axis is critical. Depletion of USP1 increases K48-linked ubiquitinated-RPS16, leading to proteasome-dependent RPS16 degradation. USP1 depletion mimics RPS16 deficiency, inhibiting growth and metastasis of HCC cells, while re-expression of RPS16 restores oncogenic-like activity in USP1-deficient HCC cells. High expression of USP1 and RPS16 in liver tissue is a poor survival prognostic factor for HCC patients [1]. Also, in HCC, SNS-023 can induce degradation of RPS16, leading to cell cycle arrest, apoptosis, and suppression of cell proliferation and migration. The EGFR-AKT-USP1 axis drives the growth of HCC with RPS16 as a crucial substrate [3].

In influenza A virus infection, microRNA let-7 targets the 3'-untranslated region of Rps16, decreasing its expression. Knocking down Rps16 increases type I interferon expression and inhibits viral replication [4].

In Alzheimer's disease patients, RPS16, along with many other ribosomal proteins, is significantly upregulated in brain capillaries but not in brain parenchyma, suggesting a role in the ribosome complex-related processes at the blood-brain barrier [5].

In conclusion, Rps16 is essential for translation initiation and protein synthesis. Through gene-related studies in models like those of HCC, influenza A virus infection, and Alzheimer's disease, its role in disease-related biological processes has been revealed. These findings provide insights into potential therapeutic strategies for these diseases.