Rpl7l1, encoding 60S Ribosomal Protein L7-Like 1, is involved in ribosome biogenesis, which is associated with cancer development [1,3]. It has been implicated in multiple biological processes. In mouse studies, it is required for blastocyst formation [4].

In cancer research, pan-cancer analysis shows Rpl7l1 was overexpressed in nine tumor types. Its gene mutation, tumor microenvironment and methylation modification play a key role in patient prognosis. High expression of Rpl7l1 was associated with TMB, MSI, LOH especially in LIHC and HNSC, and experimentally verified to promote the proliferation and migration of tumor cells [1].

In a study on pig abdominal subcutaneous fat deposition, Rpl7l1 was identified as one of the hub genes in a protein-protein interaction network, and a potential obese-specific biomarker [2].

In lung adenocarcinoma, it was among the hub genes overexpressed and enriched in RNA processing, ribosome biogenesis, and mitochondrial translation, with high-expression cohorts having poor overall survival [3].

In conclusion, Rpl7l1 is crucial for blastocyst formation in mice. In diseases, it shows potential as a biomarker in cancer and is associated with fat deposition in pigs. Research on Rpl7l1, especially through mouse models, provides insights into its role in development and disease, potentially guiding future therapeutic strategies for cancer and understanding obesity-related mechanisms [1,2,3,4].