Pbsn, often associated with prostate-related biology, is expressed in a large population of differentiated cells in the mouse prostate, along with Nkx3.1 [1]. Although its exact function is not fully detailed in the provided references, its expression pattern indicates its potential importance in the normal functioning and differentiation processes within the prostate gland. The genes in this context may be related to pathways involved in prostate cell maintenance and regeneration.

In the study of prostate cancer, the transgenic mouse models like TRAMP/Pbsn-Myc were used. The RBM22 levels were found to be down-regulated in prostate cancer (PCa) samples, and a gradual reduction of RBM22 from non-tumor to poorly differentiated PCa samples was observed in these models. RBM22 overexpression decreased aggressiveness features in vitro and in vivo, which may imply an indirect relationship between Pbsn (through the model) and PCa pathophysiology [2].

In conclusion, Pbsn is likely to be involved in the normal differentiation and function of prostate cells. The use of transgenic mouse models such as TRAMP/Pbsn-Myc has provided insights into its possible connection with prostate cancer development, suggesting that further research on Pbsn could potentially lead to a better understanding of prostate cancer mechanisms and new treatment strategies.

References:

1. Karthaus, Wouter R, Hofree, Matan, Choi, Danielle, Regev, Aviv, Sawyers, Charles L. . Regenerative potential of prostate luminal cells revealed by single-cell analysis. In Science (New York, N.Y.), 368, 497-505. doi:10.1126/science.aay0267. https://pubmed.ncbi.nlm.nih.gov/32355025/

2. Jiménez-Vacas, Juan M, Montero-Hidalgo, Antonio J, Gómez-Gómez, Enrique, Gahete, Manuel D, Luque, Raul M. 2022. Tumor suppressor role of RBM22 in prostate cancer acting as a dual-factor regulating alternative splicing and transcription of key oncogenic genes. In Translational research : the journal of laboratory and clinical medicine, 253, 68-79. doi:10.1016/j.trsl.2022.08.016. https://pubmed.ncbi.nlm.nih.gov/36089245/