USP38 inhibits colorectal cancer cell proliferation and migration via downregulating HMX3 ubiquitylation
Jun Wang, GU Yong-xing, Xueqin Yan, Jie Zhang, Jun Wang, Yong Ding
Abstract
experiment revealed HMX3 overexpression could also suppress tumor growth. Combining bioinformatics and WB analysis, we preliminarily uncovered that HMX3 was involved in apoptosis and KRAS signaling pathways. Mechanistically, Ubiquitin-specific protease 38 (USP38) was identified as a novel post-translational regulator of HMX3, which could directly interact with HMX3 to stabilize its protein expression via deubiquitination. Furthermore, the role of USP38 silencing in promoting cell proliferation, migration, and invasion of CRC cells was blocked by HMX3 overexpression. In conclusion, our findings suggested that USP38/HMX3 axis is a novel promising therapeutic candidate for CRC.
Topics & Concepts
Cancer researchColorectal cancerUbiquitinCell growthCancerMedicineBiologyInternal medicineGeneGeneticsUbiquitin and proteasome pathwaysRNA modifications and cancerCancer-related molecular mechanisms research