Rsl1d1, ribosomal L1 domain containing 1, is a member of the universal ribosomal protein uL1 family. It is involved in multiple cellular processes, and its associated pathways include those related to autophagy, cell senescence, proliferation, and iron metabolism [1,2,4]. It also plays a role in nuclear protein transport during preimplantation embryo development [3]. In cancer, especially colorectal cancer, it has been a focus of research, indicating its potential importance in disease-related biological processes [1,4,5,6,7].

In female mice with an oocyte-specific knockout of Rsl1d1, there is embryo arrest due to zygotic genome activation defects, recapitulating the phenotype of human preimplantation embryo arrest, demonstrating the vital role of Rsl1d1 in this process [3]. In colorectal cancer, Rsl1d1 knockdown inhibits cell proliferation, induces cell cycle arrest, apoptosis, and ferroptosis, and affects iron metabolism. Overexpression of Rsl1d1 promotes cancer cell proliferation, invasion, and metastasis by suppressing autophagy. It also interacts with proteins like RAN, p53, and HDM2, influencing their functions [1,4,5,6].

In conclusion, Rsl1d1 is crucial for multiple biological functions, including preimplantation embryo development and regulation of cellular processes in cancer. The oocyte-specific Rsl1d1 knockout mouse model has revealed its significance in preimplantation embryo arrest, while studies in colorectal cancer have shown its complex role in cancer progression, providing potential targets for related disease treatment.