期刊
JOURNAL OF CANCER
卷 12, 期 15, 页码 4542-4551出版社
IVYSPRING INT PUBL
DOI: 10.7150/jca.58710
关键词
GL-V9; colorectal cancer; invasion; matrix metalloproteinases; PI3K/Akt
类别
资金
- Hangzhou Peak Discipline of Gastroenterology
- Key Laboratory of Integrated Traditional Chinese and Western Medicine for Biliary and Pancreatic Diseases of Zhejiang Province
- Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province [2020E10021]
- Science and Technology Project of Hangzhou Health Commission [A20200113]
- Zhejiang Medical and Health Science and Technology Plan [WKJ-ZJ-2136 2019RC068, 2021437779]
- Hangzhou Medical and Health Science and Technology Plan [2016ZD01, OO20190610, A20200174]
GL-V9 inhibits the invasion and migration of CRC cells by suppressing the PI3K/Akt signaling pathway and MMP-2/9 axis. It may be a potential novel therapeutic agent against CRC metastasis.
Tumor distant metastasis is the primary cause of death in colorectal cancer (CRC) patients. GL-V9 is a newly synthesized flavonoid derivative with several beneficial biological functions including anti-tumor and anti-inflammation. However, the anti-metastatic effect of GL-V9 and related mechanisms in CRC remains unknown. In this study, the anti-invasive and anti-migratory activities of GL-V9 were investigated in CRC cells. Using MTT assay, cell wound healing assay, and transwell migration assay, we showed that GL-V9 suppressed CRC cell viability, migration, and invasion in a concentration-dependent manner. In addition, the protein expression levels as well as activities of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) were significantly reduced after GL-V9 treatment. Further analysis of the underlying mechanism revealed that GL-V9 inhibited PI3K/Akt signaling pathway upstream of MMP-2 and MMP-9. In conclusion, our study demonstrated that GL-V9 could suppress CRC cell invasion and migration through PI3K/Ak and MMP-2/9 axis. Therefore, GL-V9 might be a potential novel therapeutic agent against CRC metastasis.
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