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
Serpin peptidase inhibitor clade H member 1 (SERPINH1) was initially recog
To investigate the effects of SERPINH1 on CRC cells and its specific mechanism.
Quantitative real-time polymerase chain reaction, western blotting analysis, The Cancer Genome Atlas data mining and immunohistochemistry were employed to examine SERPINH1 expression in CRC cell lines and tissues. A series of in-vitro assays were performed to demonstrate the function of SERPINH1 and its possible mechanisms in CRC.
SERPINH1 demonstrated elevated expression levels in both CRC cells and tissues, manifested at both mRNA and protein tiers. Elevated SERPINH1 levels correlated closely with advanced T stage, lymph node involvement, and distant metastasis, exhibiting a significant association with poorer overall survival among CRC pa
These findings imply a crucial involvement of SERPINH1 in the advancement and escalation of CRC, potentially positioning it as a novel candidate for prognostic assessment and therapeutic intervention in CRC management.
Core Tip: The expression of serpin peptidase inhibitor clade H member 1 (SERPINH1) was observed to be elevated in both colorectal cancer (CRC) cells and tissues at mRNA and protein levels. Increased SERPINH1 expression demonstrated a close association with the T stage, lymph node status, and distant metastasis in CRC patients, displaying a significant correlation with poor overall survival. Subsequent investigations revealed that the overexpression of SERPINH1 markedly enhanced the in vitro proliferation, invasion, and migration capabilities of CRC cells. Conversely, the knockdown of SERPINH1 resulted in the opposite effects. In addition, our study validated that the overexpression of SERPINH1 could stimulate the G1/S phase cell cycle transition through the activation of the phosphatidylinositol 3-kinase (PI3