TRIM28 and Endogenous Retroviral Element Expression in Prostate Development and Disease
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p53f/f (NPp53) genetically engineered mouse model of prostate cancer with Trim28 knockout to study how TRIM28 deletion affects prostate cancer cells in an immunocompetent microenvironment. Intriguingly, we observed that TRIM28 regulated cellular plasticity in prostate cancer cells, and its deletion led to an upregulation of endogenous retroviral elements and changes to the tumor microenvironment that supported tumor growth. We also observed that TRIM28 function was independent of androgen receptor signaling, which is typically inhibited as standard of care for prostate cancer. Furthermore, we performed lineage tracing and genetic knockout of Trim28 in prostate luminal cells during organogenesis and in homeostasis. In prostate luminal cells we found that TRIM28 was required during development but not in normal adult prostates. In conclusion, our characterization of TRIM28 requirements across multiple cellular contexts in the prostate has provided valuable insight into TRIM28 function in the prostate.
Ptenf/f
The tripartite motif containing 28 (TRIM28) protein performs key functions in transcriptional repression, retroviral element silencing, genomic stability, and cellular plasticity. TRIM28 expression is elevated in advanced prostate cancers, and knockdown in human prostate cancer cell lines slows tumor growth. We utilized the Nkx3.1-CreERT2/+
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