Table 1 Represents diseases associated to USP6 dysregulation.
From: Physiological roles and therapeutic implications of USP6
Disease | Protein (USP6) | Target | Mechanism | Reference |
|---|---|---|---|---|
Aneurysmal bone cyst | Overexpressed | TRAF6, c-junction | Overexpressed USP6 bind with TRAF6, and c-junction to regulate aneurysmal bone cyst. | [52] |
Nodular fasciitis | Overexpressed | TRAF6, c-junction collagen 1 | Overexpressed USP6 bind with TRAF6, and c-junction, and collagen 1 and cause nodular fasciitis. | |
Cranial fasciitis | Overexpressed | Wnt pathway | USP6 as an oncogene promotes cancer cell growth, invasion, by regulating Wnt pathway. | [58] |
Breast cancer | Overexpressed | transforming growth factor beta | USP6 regulate transforming growth factor beta (TGFβ) signaling, has a well-documented role in mediating epithelial-to-mesenchymal transition (EMT), tumor progression and metastasis in breast cancer. | [64] |
Colon cancer | Overexpressed | GOLPH3 and COAD | Overexpression of USP6 promoted COAD cell viability, inhibited apoptosis, and accelerated the growth of transplanted tumors growth in vitro and in vivo by deubiquitinating GOLPH3 | [69] |
Colorectal cancer | Overexpressed | Wnt/β-catenin pathway | USP6 with high expression in CRC tissues regulates CRC cell proliferation | [73] |
Memory dysfunction | Overexpressed | NMDAR, GluN1 | USP6 SP6 enhances GluN1. NMDAR stability to promote synaptic function and cognition | [79] |
Chronic myeloid leukemia | Overexpressed | GLS1 | Overexpression of USP6 reduces GLS1 ubiquitination, preventing breakdown and allowing for continued glutamine metabolism. This metabolic adaptation leads to CML cells’ resistance to imatinib-induced apoptosis |
