Published online May 15, 2024. doi: 10.4251/wjgo.v16.i5.1890
Peer-review started: October 19, 2023
First decision: December 29, 2023
Revised: January 10, 2024
Accepted: March 14, 2024
Article in press: March 14, 2024
Published online: May 15, 2024
Processing time: 202 Days and 21.5 Hours
The clinical significance and biological role of serpin peptidase inhibitor clade H member 1 (SERPINH1) in colorectal cancer (CRC) remains poorly understood.
To investigate the effect of SERPINH1 on CRC cells and its specific mechanism.
To further study the specific role and mechanism of SERPINH1 in CRC and provide theoretical basis for further using SERPINH1 to improve the survival rate of CRC patients.
SERPINH1 expression in CRC cell lines and tissues was evaluated using quantitative real-time polymerase chain reaction, western blotting analysis, data mining from The Cancer Genome Atlas, and immunohistochemistry. A battery of in vitro experiments was conducted to elucidate the role of SERPINH1 and its potential mechanisms in CRC.
Our study reveals the potential for SERPINH1 to be negatively correlated with fatty acid metabolism and promote CRC progression by activating the phosphatidylinositol 3-kinase (PI3K)/AKT/mechanistic target of rapamycin (mTOR) and PI3K/AKT/FOXO1 pathways. Considering that FOXO1 and glycogen synthase kinase (GSK)-3β phosphorylation can inhibit fatty acid metabolism, which is partly mediated by CD36, this may be our next research direction.
Our study uncovered the significance of SERPINH1 in promoting CRC proliferation and metastasis by activating the PI3K/Akt/mTOR pathway. This work contributes to our understanding of the molecular mechanisms underlying CRC progression and offers a potential avenue for the development of targeted therapies.
Our study revealed the potential for SERPINH1 to be negatively correlated with fatty acid metabolism and promoted CRC progression by activating the PI3K/AKT/mTOR and PI3K/AKT/FOXO1 pathways. Considering that FOXO1 and GSK-3β phosphorylation could inhibit fatty acid metabolism, which is partly mediated by CD36, this may be our next research direction.