Rpl7l1, 60S Ribosomal Protein L7-Like 1, is associated with ribosome biogenesis, which is fundamental for protein synthesis, a process essential for cell growth, development, and function. It has been implicated in multiple biological processes including embryonic development, skeletal muscle-related functions, and may be involved in pathways like RNA processing and ribosome biogenesis [1,2,3,4]. Genetic models, such as mouse models, are valuable for studying its functions.

In a mouse model, functional knockdown of Rpl7l1 led to normal morula development but failure in blastocyst formation, specifically the inability to form a blastocoel cavity or differentiated trophectoderm, indicating its crucial role in mammalian pre-implantation development [4].

In pan-cancer analysis, Rpl7l1 was overexpressed in nine tumor types. Its gene mutation, tumor microenvironment, and methylation modification played a key role in patient prognosis. High expression of Rpl7l1 was associated with TMB, MSI, LOH especially in LIHC and HNSC, and experiments verified its promotion of tumor cell proliferation and migration [1].

In a pig study, Rpl7l1 was identified as one of the hub genes in a protein-protein interaction network related to abdominal subcutaneous fat deposition, suggesting its potential role in fat-related metabolism [2].

In lung adenocarcinoma, Rpl7l1 was among the hub genes overexpressed and enriched in RNA processing, ribosome biogenesis, and mitochondrial translation, which are critical in tumor progression [3].

In conclusion, Rpl7l1 is essential for mammalian blastocyst formation. Its abnormal expression is related to cancer development, influencing patient prognosis and tumor cell behaviors. Also, it may be involved in fat-related metabolism in pigs. Studies on Rpl7l1 using gene-knockout or other genetic mouse models contribute to understanding its functions in development and disease, especially in cancer-related areas.