Rpl27, encoding ribosomal protein L27, is involved in pre-rRNA processing and erythropoiesis [4,5]. It is also associated with ribosome complex formation, which is crucial for protein synthesis, a fundamental biological process [3]. Genetic models can be used to further explore its function.

Knockdown of Rpl27 in human colorectal cancer cell lines HCT116 and HT29 suppressed cell proliferation, cell cycle progression, and induced apoptotic cell death. In nude mice, targeting Rpl27 inhibited the growth of human CRC xenografts. This was accompanied by down-regulation of polo-like kinase 1 (PLK1) and G2/M-associated regulators, reducing the migration, invasion, and sphere-forming capacity of CRC cells [1].

In human liver cancer cell lines SNU449 and HepG2, Rpl27 knockdown decreased cell viability, proliferation rate, and increased apoptotic cells, suggesting Rpl27 is important for HCC cell proliferation and apoptosis [2].

In Diamond-Blackfan anemia, mutations in Rpl27 were identified. In vitro knockdown of Rpl27 expression disturbed pre-ribosomal RNA processing, and zebrafish models of rpl27 mutations showed impairments of erythrocyte production [5]. A case of Diamond-Blackfan anemia was associated with a digenic interaction between non-allelic RPS19 and RPL27 variants [6].

In conclusion, Rpl27 is essential for processes like pre-rRNA processing, erythropoiesis, and cell proliferation. Studies using gene knockdown in cell lines and animal models have revealed its significant role in diseases such as colorectal cancer, liver cancer, and Diamond-Blackfan anemia, providing potential therapeutic targets for these diseases.