SYNCRIP, also known as hnRNP Q, is an RNA-binding protein belonging to the cellular heterogeneous nuclear ribonucleoprotein (hnRNP) family. It is involved in multiple biological processes such as post-transcriptional regulation, miRNA biogenesis, and proteostasis maintenance. It participates in pathways related to cell development, homeostasis, and cancer-related processes, making it of great biological importance. Genetic models, like knockout mouse models, are valuable tools for studying its functions [2,3,4].

Using a conditional knockout mouse model, it was revealed that SYNCRIP is required for maintaining blood homeostasis, especially after regenerative stress. Loss of SYNCRIP led to a failure in proteome homeostasis in hematopoietic stem cells (HSCs), increased protein synthesis, and endoplasmic reticulum stress [2]. In prostate cancer cells, loss of SYNCRIP unleashed APOBEC-driven mutagenesis, which contributed to tumor heterogeneity and resistance to androgen receptor (AR)-targeted therapy. APOBEC3B, overactivated in SYNCRIP-deficient cells, was identified as a key mutator causing driver mutations in genes like FOXA1 and EP300 [1].

In conclusion, SYNCRIP plays essential roles in maintaining blood homeostasis and in cancer-related processes. The use of KO/CKO mouse models has been crucial in revealing its role in these areas, providing insights into how SYNCRIP-related dysfunctions can lead to diseases such as hematopoietic disorders and prostate cancer, and potentially guiding future therapeutic strategies.