β2-Chimaerin Deficiency Favors Polyp Growth in the Colon of Apc<sup>Min/+</sup> Mice
A Rho-GTPases are pivotal regulators of key cellular processes implicated in colorectal cancer (CRC) progression, yet the roles of their regulatory proteins, particularly GTPase-activating proteins (GAPs), remain poorly understood. This study focuses on β2-chimaerin, a Rac1-specific GAP, in Apc-driv...
Saved in:
| Main Authors: | , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2025-02-01
|
| Series: | Molecules |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1420-3049/30/4/824 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Summary: | A Rho-GTPases are pivotal regulators of key cellular processes implicated in colorectal cancer (CRC) progression, yet the roles of their regulatory proteins, particularly GTPase-activating proteins (GAPs), remain poorly understood. This study focuses on β2-chimaerin, a Rac1-specific GAP, in Apc-driven tumorigenesis using the ApcMin/+ mouse model. We demonstrate that β2-chimaerin deficiency selectively promotes the growth of colonic polyps without influencing small intestinal polyp formation. Mechanistically, β2-chimaerin loss is associated with enhanced ERK phosphorylation, while canonical Wnt/β-catenin and E-cadherin pathways remain unaffected, suggesting its specific involvement in modulating proliferative signaling in the colon. Consistent with its tumor-suppressive role, bioinformatics analyses reveal that low β2-chimaerin expression correlates with poor prognosis in CRC patients. This study expands the understanding of Rho-GTPase regulatory mechanisms in intestinal tumorigenesis, providing a basis for future therapeutic strategies targeting Rho-GTPase pathways in CRC. |
|---|---|
| ISSN: | 1420-3049 |