TRIM58 is an E3 ubiquitin ligase with dual roles in erythropoiesis and tumor suppression. In erythroid cells, TRIM58 is induced during late erythropoiesis and directly ubiquitinates dynein intermediate chains (DYNC1LI1/DYNC1LI2), promoting proteasome-dependent degradation of the dynein holoprotein complex 1. This degradation is essential for erythroblast enucleation through regulation of nuclear polarization and positioning 1. Beyond erythropoiesis, TRIM58 functions as a tumor suppressor across multiple cancer types. In gastric cancer, TRIM58 suppresses tumor growth by ubiquitinating and degrading β-catenin, thereby inactivating Wnt signaling and reducing proliferation markers 2. In colorectal cancer, TRIM58 inhibits the AKT signaling pathway through RECQL4 ubiquitination 3. In non-small cell lung cancer, TRIM58 promotes ZEB1 degradation via the ubiquitin-proteasome pathway, suppressing epithelial-to-mesenchymal transition and metastasis 4. Low TRIM58 expression correlates with poor prognosis in NSCLC patients 5. Additionally, TRIM58 plays an immune regulatory role in myeloid cells, negatively regulating TLR2 signaling to restrain intestinal mucosal inflammation; TRIM58 dysfunction contributes to ulcerative colitis pathogenesis 6. These findings position TRIM58 as a therapeutic target for erythroid-selective protein degradation and cancer treatment 7.