Detected method: |
Q
M
|
Detected method confidence |
High
|
Expression pattern: |
|
Associated gene: |
USF2 |
Associated microRNA: |
- |
Biological function: |
Ectopic expression of circACTN4 strikingly facilitated the growth, invasion, and metastasis of breast cancer cells in vitro and in vivo |
Molecular mechanism: |
circACTN4 could competitively bind to far upstream element binding protein 1 (FUBP1) to prevent the combination between FUBP1 and FIR, thereby activating MYC transcription and facilitating tumor progression of breast cancer |
Survival: |
poor |
Supported
No.: |
1 |
Description: |
Our findings uncover a pivotal mechanism that circACTN4 mediated by USF2 might interact with FUBP1 to promote the occurrence and development of breast cancer via enhancing the expression of MYC. CircACTN4 could be a novel potential target for diagnosis and treatment of breast cancer. |