Jian Yun Qing Hua Decoction inhibits malignant behaviors of gastric carcinoma cells via COL12A1 mediated ferroptosis signal pathway DOI Creative Commons
Baoxinzi Liu, Yu Li, Yuanyuan Xu

et al.

Chinese Medicine, Journal Year: 2023, Volume and Issue: 18(1)

Published: Sept. 12, 2023

Abstract Background Jian Yun Qing Hua Decoction (JYQHD), a traditional Chinese medicine decoction, which has been applied in the treatment of gastric cancer (GC). We attempt to confirm anti-gastric effect JYQHD and explore mechanism JYQHD. Methods Acute toxicity test was used understand studied expression prognostic outcome COL12A1 within GC tissues through network databases. Using several web-based databases, we analyzed major components targets JYQHD, as well known therapeutic cancer. The Venn diagram utilized obtain overlapped genes. Lentiviral vector, shRNAs plasmids, were transfect cells. Cell counting kit-8 (CCK8), sphere formation, malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS), Fe 2+ , transmission electron microscopy (TEM), quantitative Real-Time Polymerase Chain Reaction (qRT-PCR), Western-Blot (WB), immunohistochemical (IHC) assays employed investigate role GC. Results results showed that non-toxic safe. inhibited growth formation ability inducing ferroptosis cells, suppressed cells induced subcutaneous xenograft tumor growth. highly expressed tissues, indicating poor prognosis. specifically enhanced cell progression stemness via suppressing ferroptosis. down-regulated order suppress Conclusion development by inhibiting pathway mediated COL12A1.

Language: Английский

Ferroptosis and its role in gastric and colorectal cancers DOI Open Access
Jinxiu Hou, Bo Wang, Jing Li

et al.

Korean Journal of Physiology and Pharmacology, Journal Year: 2024, Volume and Issue: 28(3), P. 183 - 196

Published: April 29, 2024

Ferroptosis is a novel mechanism of programmed cell death, characterized by intracellular iron overload, intensified lipid peroxidation, and abnormal accumulation reactive oxygen species, which ultimately resulting in membrane impairment demise.Research has revealed that cancer cells exhibit greater demand for compared to normal cells, indicating potential susceptibility ferroptosis.Stomach colorectal cancers are common gastrointestinal malignancies, their elevated occurrence mortality rates render them global health concern.Despite significant advancements medical treatments, certain unfavorable consequences drug resistance persist.Consequently, directing attention towards the phenomenon ferroptosis gastric holds promise enhancing therapeutic efficacy.This review aims elucidate intricate cellular metabolism associated with ferroptosis, encompassing amino acid metabolism, as well metabolic processes.Furthermore, significance context thoroughly examined discussed.

Language: Английский

Citations

3

Ferroptosis, a therapeutic target for cardiovascular diseases, neurodegenerative diseases and cancer DOI Creative Commons
Yinghui Li, Cui-Yun Liu, Bo Fang

et al.

Journal of Translational Medicine, Journal Year: 2024, Volume and Issue: 22(1)

Published: Dec. 22, 2024

The identification of ferroptosis represents a pivotal advancement in the field cell death research, revealing an entirely novel mechanism cellular demise and offering new insights into initiation, progression, therapeutic management various diseases. Ferroptosis is predominantly induced by intracellular iron accumulation, lipid peroxidation, or impairments antioxidant defense system, culminating membrane rupture consequent death. Studies have associated with wide range diseases, enhancing our comprehension its underlying mechanisms, we can formulate innovative strategies, thereby providing renewed hope for patients.

Language: Английский

Citations

2

Identification and verification of ferroptosis-related genes in gastric intestinal metaplasia DOI Creative Commons
Biao Song, Tingting Li, Yi Zhang

et al.

Frontiers in Genetics, Journal Year: 2023, Volume and Issue: 14

Published: April 18, 2023

Background: Gastric intestinal metaplasia (IM) is the key link of gastric precancerous lesions. Ferroptosis a novel form programmed cell death. However, its impact on IM unclear. The focus this study to identify and verify ferroptosis-related genes (FRGs) that may be involved in by bioinformatics analysis. Materials methods: Differentially expressed (DEGs) were obtained from microarray dataset GSE60427 GSE78523 downloaded Gene Expression Omnibus (GEO) database. (DEFRGs) overlapping DEGs FRGs got FerrDb. DAVID database was used for functional enrichment Protein-protein interaction (PPI) analysis Cytoscape software screen hub gene. In addition, we built receiver operating characteristic (ROC) curve verified relative mRNA expression quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Finally, CIBERSORT algorithm analyze immune infiltration IM. Results: First, total 17 DEFRGs identified. Second, gene module identified considered as gene: PTGS2, HMOX1, IFNG, NOS2. Third, ROC showed HMOX1 NOS2 had good diagnostic characteristics. qRT-PCR experiments confirmed differential normal tissues. immunoassay proportion T cells regulatory (Tregs) macrophages M0 relatively higher, while CD4 memory activated dendritic lower. Conclusion: We found significant associations between IM, biomarkers therapeutic targets These results enhance our understanding contribute treatment.

Language: Английский

Citations

4

RETRACTED: Sulforaphane triggers iron overload-mediated ferroptosis in gastric carcinoma cells by activating the PI3K/IRP2/DMT1 pathway DOI Creative Commons
Jing Wen, Fan Yang,

Chengxiang Fang

et al.

Human & Experimental Toxicology, Journal Year: 2023, Volume and Issue: 42

Published: March 1, 2023

Increasing evidence indicates that prolonged exposure to sulforaphane (SFN) can improve malignancies. However, the role of iron in SFN-triggered death gastric carcinoma cells and underlying molecular mechanisms remain unclear. Thus, current study explored effects SFN on overload-mediated ferroptosis PI3K/IRP2/DMT1 pathway cells.We utilized MGC-803 cell line assess whether affected metabolism this effect contributed death. Pharmacological inhibition also was performed determine mechanism overload disturbance metabolism.Our data revealed treatment altered homeostasis led vitro. Interestingly, SFN-stimulated resulted from ferroptosis, a recently identified iron-dependent form regulated Furthermore, an chelator, deferiprone, ameliorated mitochondrial dysfunction reduced overload. In addition, we found by signaling pathway.We discovered might be involved cells. Blockade axis could provide feedback SFN-induced protect tumor growth.

Language: Английский

Citations

4

Jian Yun Qing Hua Decoction inhibits malignant behaviors of gastric carcinoma cells via COL12A1 mediated ferroptosis signal pathway DOI Creative Commons
Baoxinzi Liu, Yu Li, Yuanyuan Xu

et al.

Chinese Medicine, Journal Year: 2023, Volume and Issue: 18(1)

Published: Sept. 12, 2023

Abstract Background Jian Yun Qing Hua Decoction (JYQHD), a traditional Chinese medicine decoction, which has been applied in the treatment of gastric cancer (GC). We attempt to confirm anti-gastric effect JYQHD and explore mechanism JYQHD. Methods Acute toxicity test was used understand studied expression prognostic outcome COL12A1 within GC tissues through network databases. Using several web-based databases, we analyzed major components targets JYQHD, as well known therapeutic cancer. The Venn diagram utilized obtain overlapped genes. Lentiviral vector, shRNAs plasmids, were transfect cells. Cell counting kit-8 (CCK8), sphere formation, malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS), Fe 2+ , transmission electron microscopy (TEM), quantitative Real-Time Polymerase Chain Reaction (qRT-PCR), Western-Blot (WB), immunohistochemical (IHC) assays employed investigate role GC. Results results showed that non-toxic safe. inhibited growth formation ability inducing ferroptosis cells, suppressed cells induced subcutaneous xenograft tumor growth. highly expressed tissues, indicating poor prognosis. specifically enhanced cell progression stemness via suppressing ferroptosis. down-regulated order suppress Conclusion development by inhibiting pathway mediated COL12A1.

Language: Английский

Citations

4