Academic Journal
Isorhamnetin Suppresses Human Gastric Cancer Cell Proliferation through Mitochondria-Dependent Apoptosis
| Title: | Isorhamnetin Suppresses Human Gastric Cancer Cell Proliferation through Mitochondria-Dependent Apoptosis |
|---|---|
| Authors: | Yehua Li, Baoqiang Fan, Ning Pu, Xue Ran, Tiancheng Lian, Yifan Cai, Wei Xing, Kun Sun |
| Source: | Molecules, Vol 27, Iss 16, p 5191 (2022) |
| Publisher Information: | MDPI AG, 2022. |
| Publication Year: | 2022 |
| Collection: | LCC:Organic chemistry |
| Subject Terms: | isorhamnetin, mitochondria, apoptosis, gastric cancer, transcriptome, Organic chemistry, QD241-441 |
| More Details: | Derivates of natural products have been wildly utilized in the treatment of malignant tumors. Isorhamnetin (ISO), a most important active ingredient derived from flavonoids, shows great potential in tumor therapy. However, the therapeutic effects of ISO on gastric cancer (GC) remain unclear. Here, we demonstrate that ISO treatment dramatically inhibited the proliferation of two types of GC cells (AGS-1 and HGC-27) both in vitro and in vivo in time- and dose-dependent manners. These results are consistent with the transcriptomic analysis of ISO-treated GC cells, which yielded hundreds of differentially expressed genes that were enriched with cell growth and apoptosis. Mechanically, ISO treatment initiated the activation of caspase-3 cascade and elevated the expression of mitochondria-associated Bax/Bcl-2, cytosolic cytochrome c, followed by the activation of the cleavage of caspase-3 as well as poly ADP-ribose polymerase (PARP), resulting in the severe reduction of the mitochondrial potential and the accumulation of reactive oxygen species (ROS), while pre-treatment of the caspase-3 inhibitor could block the anti-tumor effect. Therefore, these results indicate that ISO treatment induces the apoptosis of GC cells through the mitochondria-dependent apoptotic pathway, providing a potential strategy for clinical GC therapy. |
| Document Type: | article |
| File Description: | electronic resource |
| Language: | English |
| ISSN: | 27165191 1420-3049 |
| Relation: | https://www.mdpi.com/1420-3049/27/16/5191; https://doaj.org/toc/1420-3049 |
| DOI: | 10.3390/molecules27165191 |
| Access URL: | https://doaj.org/article/5c730d225f464613b29c08563e92af11 |
| Accession Number: | edsdoj.5c730d225f464613b29c08563e92af11 |
| Database: | Directory of Open Access Journals |
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| ISSN: | 27165191 14203049 |
|---|---|
| DOI: | 10.3390/molecules27165191 |
| Published in: | Molecules |
| Language: | English |