| General information | Literature | Expression | Regulation | Mutation | Homolog | Interaction |
Basic Information | |
|---|---|
Gene ID | 10054 |
Name | UBA2 |
Synonymous | ubiquitin-like modifier activating enzyme 2;UBA2;ubiquitin-like modifier activating enzyme 2 |
Definition | SUMO-1 activating enzyme subunit 2|SUMO-activating enzyme subunit 2|SUMO1 activating enzyme subunit 2|UBA2, ubiquitin-activating enzyme E1 homolog|anthracycline-associated resistance ARX|ubiquitin-like 1-activating enzyme E1B|ubiquitin-like modifier-activ |
Position | 19q12 |
Gene type | protein-coding |
Title | Abstract |
| breast cancer | Myc is an oncogenic transcription factor frequently dysregulated in human cancer. To identify pathways supporting the Myc oncogenic program, we used a genome-wide RNA interference screen to search for Myc-synthetic lethal genes and uncovered a role for the SUMO-activating enzyme (SAE1/2). Loss of SAE1/2 enzymatic activity drives synthetic lethality with Myc. Inactivation of SAE2 leads to mitotic catastrophe and cell death upon Myc hyperactivation. Mechanistically, SAE2 inhibition switches a transcriptional subprogram of Myc from activated to repressed. A subset of these SUMOylation-dependent Myc switchers (SMS genes) is required for mitotic spindle function and to support the Myc oncogenic program. SAE2 is required for growth of Myc-dependent tumors in mice, and gene expression analyses of Myc-high human breast cancers suggest that low SAE1 and SAE2 abundance in the tumors correlates with longer metastasis-free survival of the patients. Thus, inhibition of SUMOylation may merit investigation as a possible therapy for Myc-driven human cancers. |