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

Overcoming cancer chemotherapy resistance by the induction of ferroptosis DOI
Yumin Wang,

Xiaorui Wu,

Ren Zhao

et al.

Drug Resistance Updates, Journal Year: 2022, Volume and Issue: 66, P. 100916 - 100916

Published: Dec. 29, 2022

Language: Английский

Citations

171
Ferroptosis-Based Therapeutic Strategies toward Precision Medicine for Cancer DOI

Tianqi Shi,

Xiaofei Chen, Huihui Ti

et al.

Journal of Medicinal Chemistry, Journal Year: 2024, Volume and Issue: 67(4), P. 2238 - 2263

Published: Feb. 2, 2024

Ferroptosis is a type of iron-dependent programmed cell death characterized by the dysregulation iron metabolism and accumulation lipid peroxides. This nonapoptotic mode implicated in various physiological pathological processes. Recent findings have underscored its potential as an innovative strategy for cancer treatment, particularly against recalcitrant malignancies that are resistant to conventional therapies. article focuses on ferroptosis-based therapeutic strategies precision covering molecular mechanisms ferroptosis, four major types ferroptosis inducers their inhibitory effects diverse carcinomas, detection fluorescent probes, implementation image-guided therapy. These state-of-the-art tactics manifested enhanced selectivity efficacy malignant carcinomas. Given administration therapy still at burgeoning stage, some challenges future perspectives discussed clinical translation into treatment.

Language: Английский

Citations

12
Interplay of CD36, autophagy, and lipid metabolism: insights into cancer progression DOI
Yuxuan Yang, Xiaokun Liu, Di Yang

et al.

Metabolism, Journal Year: 2024, Volume and Issue: 155, P. 155905 - 155905

Published: March 26, 2024

Language: Английский

Citations

11
POU6F1 promotes ferroptosis by increasing lncRNA-CASC2 transcription to regulate SOCS2/SLC7A11 signaling in gastric cancer DOI Creative Commons
Jingyun Wang,

Qiaoyu Jia,

Shuqin Jiang

et al.

Cell Biology and Toxicology, Journal Year: 2024, Volume and Issue: 40(1)

Published: Jan. 25, 2024

Abstract Objective This study investigated the effect and mechanism of POU6F1 lncRNA-CASC2 on ferroptosis gastric cancer (GC) cells. Methods GC cells treated with erastin RSL3 were detected for ferroptosis, reactive oxygen species (ROS) level, cell viability. The expression levels POU6F1, lncRNA-CASC2, SOCS2, ferroptosis-related molecules (GPX4 SLC7A11) also measured. regulations among FMR1, SLC7A11 determined. Subcutaneous tumor models established, in which expressions Ki-67, GPX4 by immunohistochemistry. Results patients decreased had lower survival rate. Overexpression or proliferation GSH cells, addition to increasing total iron, Fe2+, MDA, ROS levels. directly binds promoter promote its transcription. LncRNA-CASC2 can target FMR1 increase SOCS2 mRNA stability ubiquitination degradation activate signaling. Knockdown inhibited sensitivity reversed effects overexpression Conclusion Transcription factor expression, while upregulated increases targeting thereby inhibiting signaling inhibit progression.

Language: Английский

Citations

10
HDAC inhibitors activate lipid peroxidation and ferroptosis in gastric cancer DOI Creative Commons
Robert Jenke, Denys Oliinyk,

Tamara Zenz

et al.

Biochemical Pharmacology, Journal Year: 2024, Volume and Issue: 225, P. 116257 - 116257

Published: May 4, 2024

Gastric cancer remains among the deadliest neoplasms worldwide, with limited therapeutic options. Since efficacies of targeted therapies are unsatisfactory, drugs broader mechanisms action rather than a single oncogene inhibition needed. Preclinical studies have identified histone deacetylases (HDAC) as potential targets in gastric cancer. However, mechanism(s) HDAC inhibitors (HDACi) only partially understood. This is particularly true regard to ferroptosis an emerging concept cell death. In panel lines different molecular characteristics, tumor inhibitory effects HDACi were studied. Lipid peroxidation levels measured and proteome analysis was performed for in-depth characterization alterations upon inhibition. on important genes validated mRNA protein level. Upon treatment, lipid found increased all lines. Class I (VK1, entinostat) showed same toxicity profile pan-HDACi vorinostat. Proteome revealed significant concordant expression proteins related induction. Key enzymes like ACSL4, POR or SLC7A11 distinct their patterns, providing explanation peroxidation. Results also confirmed primary human tissue cultures relevant ex vivo model. We identify induction new mechanism class Notably, these findings independent genetic background lines, thus introducing more general principle.

Language: Английский

Citations

10
Mendelian randomization analysis of plasma proteins reveals potential novel tumor markers for gastric cancer DOI Creative Commons

Wenhai Fan,

Zhenjiang Wu, Shenghao Xu

et al.

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: Jan. 28, 2025

This study aimed to elucidate the potential causal relationship between 4,907 plasma proteins and risk of gastric cancer using a two-sample Mendelian randomization approach. We utilized genome-wide association (GWAS) data perform analyses, treating as exposure factors outcome. Instrumental variables for were selected based on strongly correlated SNPs identified through processing screening GWAS provided by deCode database. employed set statistical methods centered inverse variance weighting (IVW) analysis estimate odds ratios (ORs) effects these susceptibility. According IVW method, 14 associated with (p < 0.005). Specifically, CHST15 (OR = 0.7553, 95% CI 0.6346 − 0.8988), L1CAM 0.7230, 0.5876 0.8896), FTMT 0.8246, 0.7241 0.9391), PMM2 0.5767, 0.3943 0.8433) negatively GASTRIC CANCER, whereas ABO 1.1868, 1.0638 1.3240), FAM3D 1.2109, 1.0850 1.3515), FAM3B 1.2988, 1.0953 1.5402), ADH7 1.3568, 1.1044 1.6670), MAP1LC3A 1.3704, 1.1194 1.6778), PGLYRP1 1.4071, 1.1235 1.7623), PDE5A 1.7446, 1.2693 2.3978), GLUL 3.1203, 1.5017 6.4839), NFE2L1 3.1759, 1.6163 6.2402), MAFG 3.1945, 1.5329 6.6575) positively correlated. Convergent results from Weighted Median MR-Egger analyses confirmed associations. Reverse indicated that does not significantly alter levels > 0.05). Sensitivity including assessments heterogeneity horizontal pleiotropy, robustness reliability our findings without significant bias. Pathway enrichment gene expression proteins, GO KEGG pathways, revealed CHST15, L1CAM, FTMT, may serve protective against cancer, while ABO, FAM3D, FAM3B, ADH7, MAP1LC3A, PGLYRP1, PDE5A, GLUL, NFE2L1, contribute pathogenesis. These highlight complex biological interactions tumorigenesis, providing valuable insights preventive therapeutic strategies in malignancy management.

Language: Английский

Citations

1
Qizhu Jianwei decoction triggers ferroptosis by exosome-mediated miR-199-3p/ACSL4 signaling pathways DOI
Xinyi Dai, Yanqin Hu, Cheng Sun

et al.

Journal of Ethnopharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 119529 - 119529

Published: Feb. 1, 2025

Language: Английский

Citations

1
Glycine regulates lipid peroxidation promoting porcine oocyte maturation and early embryonic development DOI
Lepeng Gao, Chang Zhang, Yingying Zheng

et al.

Journal of Animal Science, Journal Year: 2022, Volume and Issue: 101

Published: Dec. 27, 2022

Abstract In vitro-cultured oocytes are separated from the follicular micro-environment in vivo and more vulnerable than to changes external environment. This vulnerability disrupts homeostasis of intracellular environment, affecting oocyte meiotic completion, subsequent embryonic developmental competence vitro. Glycine, one main components glutathione (GSH), plays an important role protection porcine However, protective mechanism glycine needs be further clarified. Our results showed that supplementation promoted cumulus cell expansion maturation. Detection development ability significantly increased cleavage rate blastocyst during vitro fertilization (IVF). SMART-seq revealed this effect was related glycine-mediated regulation membrane structure function. Exogenous addition levels anti-oxidant GSH expression anti-oxidant-related genes (glutathione peroxidase 4 [GPX4], catalase [CAT], superoxide dismutase 1 [SOD1], 2 [SOD2], mitochondrial solute carrier family 25, member 39 [SLC25A39]), decreased lipid peroxidation caused by reactive oxygen species (ROS) reduced level malondialdehyde (MDA) enhancing functions mitochondria, peroxisomes droplets (LDs) metabolism-related factors (peroxisome proliferator activated receptor coactivator alpha [PGC-1α], peroxisome proliferator-activated γ [PPARγ], sterol regulatory element binding factor [SREBF1], autocrine motility [AMFR], ATP). These effects ferroptosis maintained normal function membrane. suggest maturation later regulating ROS-induced metabolism, thereby protecting against biomembrane damage.

Language: Английский

Citations

29
Targeting ferroptosis in gastric cancer: Strategies and opportunities DOI

Jiahan Le,

Guangzhao Pan,

Che Zhang

et al.

Immunological Reviews, Journal Year: 2023, Volume and Issue: 321(1), P. 228 - 245

Published: Oct. 30, 2023

Summary Ferroptosis is a novel form of programmed cell death morphologically, genetically, and biochemically distinct from other pathways characterized by the accumulation iron‐dependent lipid peroxides oxidative damage. It now understood that ferroptosis plays an essential role in various biological processes, especially metabolism iron, lipids, amino acids. Gastric cancer (GC) prevalent malignant tumor worldwide with low early diagnosis rates high metastasis rates, accounting for its relatively poor prognosis. Although chemotherapy commonly used to treat GC, drug resistance often leads therapeutic outcomes. In last several years, extensive research on has highlighted significant potential GC therapy, providing promising strategy address associated standard therapies. this review, we offer summary key regulatory factors related mechanisms underlying ferroptosis. Various inducers inhibitors specifically targeting are uncovered. Additionally, explore prospective applications outcomes these agents field emphasizing their capacity improve patient population.

Language: Английский

Citations

22
Reactive Oxygen Species and H. pylori Infection: A Comprehensive Review of Their Roles in Gastric Cancer Development DOI Creative Commons
Dhiraj Kumar Sah, Archana Arjunan, Bora Lee

et al.

Antioxidants, Journal Year: 2023, Volume and Issue: 12(9), P. 1712 - 1712

Published: Sept. 2, 2023

Gastric cancer (GC) is the fifth most common worldwide and makes up a significant component of global burden. Helicobacter pylori (H. pylori) influential risk factor for GC, with International Agency Research on Cancer classifying it as Class I carcinogen GC. H. has been shown to persist in stomach acid decades, causing damage stomach’s mucosal lining, altering gastric hormone release patterns, potentially function. Epidemiological studies have that eliminating reduces metachronous cancer. Evidence shows various molecular alterations are present precancerous lesions associated an infection. However, although can cause oxidative stress-induced cancer, antioxidants being treatment exact mechanism underlying GC etiology not fully understood. This review provides overview recent research exploring pathophysiology pylori-induced stress antioxidant supplements reduce or even eliminate occurrence.

Language: Английский

Citations

17