TRIM37 augments AP-2? transcriptional activity and cellular localization via K63-linked polyubiquitination to drive breast cancer progression [ChIP-seq]

Using a proteomics approach, we identified the Tripartite Motif Containing 37 (TRIM37) as a novel transcriptional coactivator of AP-2?. We demonstrate TRIM37 facilitates AP-2? chromatin binding to regulate the AP-2? mediated transcriptional program directly. We provide evidence that TRIM37 achieves this by stimulating K63-chain-linked polyubiquitination of AP-2?, promoting protein localization from the cytoplasm to the nucleus. In clinical analyses, we find TRIM37 is upregulated in multiple breast cancer datasets, supporting our findings that TRIM37-AP-2? interaction is essential for breast cancer tumor growth. Overall, our work revealed that TRIM37 is an oncogenic coactivator of AP-2? in breast cancer and provides a novel therapeutic target for treating the disease. Overall design: ChIP-seq for TRIM37 and AP-2? in MCF-7 cells