AI Article Synopsis
- * PSMB4 is found to be highly expressed in both low- and high-grade bladder cancer, and its knockdown leads to reduced migration of cancer cells by decreasing proteins like focal adhesion kinase (FAK) and myosin light chain (MLC).
- * In addition to affecting cancer cell movement, knocking down PSMB4 lowers levels of vascular endothelial factor B (VEGF-B), which decreases blood vessel formation, showing PSMB4 as a promising target for treatments against bladder cancer.
Article Abstract
Bladder cancer (BC) is a malignant tumor of the urinary system with high mortality and recurrence rates. Proteasome subunit type 4 (PSMB4) is highly expressed and has been identified as having oncogenic properties in a variety of cancer types. This study aimed to explore the effect of PSMB4 knockdown on the survival, migration, and angiogenesis of human bladder cancer cells with different degrees of malignancy. We analyzed the effects of PSMB4 knockdown in bladder cancer cells and endothelial cells in the tumor microenvironment. PSMB4 was highly expressed in patients with low- and high-grade urothelial carcinoma. Inhibition of PSMB4 reduced protein expression of focal adhesion kinase (FAK) and myosin light chain (MLC), leading to reduced migration. Furthermore, the suppression of PSMB4 decreased the levels of vascular endothelial factor B (VEGF-B), resulting in lower angiogenic abilities in human bladder cancer cells. PSMB4 inhibition affected the migratory ability of HUVECs and reduced VEGFR2 expression, consequently downregulating angiogenesis. In the metastatic animal model, PSMB4 knockdown reduced the relative volumes of lung tumors. Our findings suggest the role of PSMB4 as a potential target for therapeutic strategies against human bladder cancer.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11122396 | PMC |
| http://dx.doi.org/10.3390/ijms25105559 | DOI Listing |
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