Published online Apr 21, 2024. doi: 10.3748/wjg.v30.i15.2155
Peer-review started: January 5, 2024
First decision: January 22, 2024
Revised: February 2, 2024
Accepted: March 14, 2024
Article in press: March 14, 2024
Published online: April 21, 2024
Processing time: 105 Days and 0.9 Hours
Necroptosis has emerged as a novel molecular pathway that can be targeted by chemotherapy agents in the treatment of cancer. OSW-1, which is derived from the bulbs of Ornithogalum saundersiae Baker, exerts a wide range of pharmacological effects.
To explore whether OSW-1 can induce necroptosis in colorectal cancer (CRC) cells, thereby expanding its range of clinical applications.
We performed a sequence of functional experiments, including Cell Counting Kit-8 assays and flow cytometry analysis, to assess the inhibitory effect of OSW-1 on CRC cells. We utilized quantitative proteomics, employing tandem mass tag label
The results revealed that OSW-1 exerted a strong inhibitory effect on CRC cells, and this effect was accompanied by a necroptosis-like morphology that was observable via TEM. OSW-1 was shown to trigger necroptosis via activation of the RIPK1/RIPK3/MLKL pathway. Furthermore, the accumulation of p62/SQSTM1 was shown to mediate OSW-1-induced necroptosis through its interaction with RIPK1.
We propose that OSW-1 can induce necroptosis through the RIPK1/RIPK3/MLKL signaling pathway, and that this effect is mediated by the RIPK1-p62/SQSTM1 complex, in CRC cells. These results provide a theoretical foundation for the use of OSW-1 in the clinical treatment of CRC.
Core Tip: Colorectal cancer (CRC) is a significant health concern worldwide, and it has severe impacts on human lives. Identifying effective drugs for CRC treatment is very important. OSW-1, which is derived from the bulbs of Ornithogalum saundersiae, exhibits potent antitumor properties. This study confirmed the inhibitory effect of OSW-1 on CRC through both in vitro and in vivo experiments. Furthermore, tandem mass tag proteomic analysis was employed to predict differentially expressed proteins and potential underlying mechanisms. Our findings suggest that OSW-1 induces necroptosis via the RIPK1/RIPK3/MLKL signaling pathway, and this effect is mediated by the RIPK1-p62/SQSTM1 complex. These results provide a theoretical foundation for the use of OSW-1 in the clinical treatment of CRC.