scholarly journals Tanshinone IIA induces ferroptosis in gastric cancer cells through p53-mediated SLC7A11 down-regulation

2020 ◽  
Vol 40 (8) ◽  
Author(s):  
Zhenhua Guan ◽  
Jing Chen ◽  
Xueliang Li ◽  
Na Dong
Keyword(s):  
Gastric Cancer ◽  
Lipid Peroxidation ◽  
Cancer Cells ◽  
Salvia Miltiorrhiza ◽  
Chinese Herb ◽  
Tanshinone Iia ◽  
Gastric Cancer Cells ◽  
P53 Expression ◽  
Anti Cancer ◽  
Pharmacologically Active

Abstract Gastric cancer represents a malignant type of cancer worldwide. Tanshinone IIA (Tan IIA), a pharmacologically active component isolated from the rhizome of the Chinese herb Salvia miltiorrhiza Bunge (Danshen), has been reported to possess an anti-cancer effect in gastric cancer. However, its mechanisms are still not fully understood. In the present study, we found that Tan IIA induced ferroptosis in BGC-823 and NCI-H87 gastric cancer cells. Tan IIA increased lipid peroxidation and up-regulated Ptgs2 and Chac1 expression, two markers of ferroptosis. Ferrostatin-1 (Fer-1), an inhibitor of lipid peroxidation, inhibited Tan IIA caused-lipid peroxidation and Ptgs2 and Chac1 expression. In addition, Tan IIA also up-regulated p53 expression and down-regulated xCT expression. Tan IIA caused decreased intracellular glutathione (GSH) level and cysteine level and increased intracellular reactive oxygen species (ROS) level. p53 knockdown attenuated Tan IIA-induced lipid peroxidation and ferroptosis. Tan IIA also induced lipid peroxidation and ferroptosis in BGC-823 xenograft model, and the anti-cancer effect of Tan IIA was attenuated by Fer-1 in vivo. Therefore, Tan IIA could suppress the proliferation of gastric cancer via inducing p53 upregulation-mediated ferroptosis. Our study have identified a novel mechanism of Tan IIA against gastric cancer, and might provide a critical insight into the application of Tan IIA in gastric cancer intervention.

scholarly journals Anti-cancer effects of newly developed chemotherapeutic agent, glycoconjugated palladium (II) complex, against cisplatin-resistant gastric cancer cells

BMC Cancer ◽  
2013 ◽  
Vol 13 (1) ◽  
Author(s):  
Mamoru Tanaka ◽  
Hiromi Kataoka ◽  
Shigenobu Yano ◽  
Hiromi Ohi ◽  
Keisuke Kawamoto ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Chemotherapeutic Agent ◽  
Gastric Cancer Cells ◽  
Anti Cancer

scholarly journals Anti-Cancer Potential of Afzelin towards AGS Gastric Cancer Cells

2021 ◽  
Vol 14 (10) ◽  
pp. 973
Author(s):  
Iwona Radziejewska ◽  
Katarzyna Supruniuk ◽  
Robert Czarnomysy ◽  
Kamila Buzun ◽  
Anna Bielawska
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Culture Medium ◽  
Mrna Level ◽  
Rt Pcr ◽  
Gastric Cancer Cells ◽  
Cell Lysates ◽  
Anti Cancer ◽  
Galectin 3 ◽  
Cancer Agent

Afzelin demonstrates anti-inflammatory and anti-cancer properties. Our purpose was to assess its influence on apoptosis, Bax, caspases, MUC1, cancer-related carbohydrate antigens, enzymes participating in their formation, and galectin-3 in AGS gastric cancer cells. A total of 60 and 120 μM afzelin was used in all experiments. Flow cytometry was applied to determine apoptotic response. Western blotting and RT PCR were used to detect the expression of mentioned factors. Flavonoid at higher concentration revealed slight apoptotic respond. Bax, caspase-3, -8, -9 increased upon afzelin action. Stimulatory effect of the flavonoid on MUC1 cytoplasmic tail and extracellular domain in cell lysates and on MUC1 gene was revealed. MUC1 release into the culture medium was inhibited by the flavonoid. The 60 μM afzelin dose stimulated GalNAcTL5 protein expression and inhibited C1GalT1. ST6GalNAcT mRNA was inhibited by both flavonoid doses. ST3GalT was inhibited by 120 μM afzelin on protein and mRNA level. Lewisa/b protein was reduced by both afzelin concentrations. FUT3 and FUT4 mRNA was inhibited by 120 μM dose of afzelin. Galectin-3 protein increased in cell lysates and decreased in culture supernatant by 60 and 120 μM flavonoid. Galectin-3 gene expression was stimulated by two used concentrations of afzelin in comparison to control. We conclude that afzelin can be considered as the potential anti-cancer agent, supporting conventional cancer treatment.

scholarly journals Chrysophanol Inhibits the Progression of Gastric Cancer by Activating NLRP3

2021 ◽  
Author(s):  
Hou Binfen ◽  
Li Zhao ◽  
Min Deng
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
Antitumor Effects ◽  
Ags Cells ◽  
Anti Cancer ◽  
Colony Forming Assay

Abstract AimGastric cancer is one of the most common malignant tumors.Chrysophanol has been reported to have antitumor effects on a variety of cancers, but the role of chrysophanol in gastric cancer remains unclear. The aim of this study was to investigate the effects of chrysophanol on proliferation, pyroptosis, migration and invasion of gastric cancer cells.MethodsMKN 28 and AGS cells were treatde with different concentrations of chrysophanol, then cell proliferation, migration,invasion and pyroptosis were decteed by CCK-8, Colony-forming assay, Wound Healing assay, Transwell and flow cytometry, respectively.Subsequently, NLRP3 siRNA was transfected into MKN 28 cells, cell proliferation pyroptosis, migration and invasion were reassessed in these transfected cells. The expression of caspase-1 and IL-1β in the downstream of NLRP3 was detected by qRT PCR and Western blot.ResultsChrysophanol significantly inhibited the proliferation of GC cells, promoted pyroptosis, inhibited cell migration and invasion, and up-regulated the expression level of NLRP3 inflammasome in GC cells. Silencing NLRP3 inhibited the effects of chrysophanol on proliferation, pyroptosis, migration and invasion of MKN 28 cells. Chrysophanol plays an anti-cancer role through high expression of NLRP3.CoclusionsChrysophanol can inhibit the proliferation, migration and invasion of gastric cancer cells by regulating NLRP3, promote the death of gastric cancer cells, and play an anti-tumor role,which is a clinical strategy with great potential for the treatment of gastric cancer.

scholarly journals Chemopreventive Activity of MGN-3/Biobran Against Chemical Induction of Glandular Stomach Carcinogenesis in Rats and Its Apoptotic Effect in Gastric Cancer Cells

2016 ◽  
Vol 15 (4) ◽  
pp. NP26-NP34 ◽  
Author(s):  
Nariman K. Badr El-Din ◽  
Salma M. Abdel Fattah ◽  
Deyu Pan ◽  
Lucilene Tolentino ◽  
Mamdooh Ghoneum
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Glandular Stomach ◽  
Chemical Induction ◽  
Gastric Cancer Cells ◽  
Ki 67 ◽  
P53 Expression ◽  
Apoptotic Effect ◽  
Stomach Carcinogenesis ◽  
Chemopreventive Activity

In the current study, we investigated the chemopreventive activity of arabinoxylan rice bran, MGN-3/Biobran, against chemical induction of glandular stomach carcinogenesis in rats. Gastric cancer was induced by carcinogen methylnitronitrosoguanidine (MNNG), and rats received MNNG alone or MNNG plus Biobran (40 mg/kg body weight) for a total of 8 months. Averaged results from 2 separate readings showed that exposure to MNNG plus Biobran caused gastric dysplasia and cancer (adenocarcinoma) in 4.5/12 rats (9/24 readings, 37.5%), with 3.5/12 rats (7/24 readings, 29.2%) showing dysplasia and 1/12 rats (8.3%) developing adenocarcinoma. In contrast, in rats treated with MNNG alone, 8/10 (80%) developed dysplasia and adenocarcinoma, with 6/10 rats (60%) showing dysplasia and 2/10 rats (20%) developing adenocarcinoma. The effect of combining both agents was also associated with significant suppression of the expression of the tumor marker Ki-67 and remarkable induction in the apoptotic gastric cancer cells via mitochondrial-dependent pathway as indicated by the upregulation in p53 expression, Bax expression, downregulation in Bcl-2 expression, an increase in Bax/Bcl-2 ratio, and an activation of caspase-3. In addition, Biobran treatment induced cell-cycle arrest in the subG1 phase, where the hypodiploid cell population was markedly increased. Moreover, Biobran treatment protected rats against MNNG-induced significant decrease in lymphocyte levels. We conclude that Biobran provides protection against chemical induction of glandular stomach carcinogenesis in rats and may be useful for the treatment of human patients with gastric cancer.

scholarly journals Integrating transcriptomics and proteomics to show that tanshinone IIA suppresses cell growth by blocking glucose metabolism in gastric cancer cells

BMC Genomics ◽  
2015 ◽  
Vol 16 (1) ◽  
pp. 41 ◽  
Author(s):  
Li-Ling Lin ◽  
Chieh-Ren Hsia ◽  
Chia-Lang Hsu ◽  
Hsuan-Cheng Huang ◽  
Hsueh-Fen Juan
Keyword(s):  
Gastric Cancer ◽  
Cell Growth ◽  
Glucose Metabolism ◽  
Cancer Cells ◽  
Tanshinone Iia ◽  
Gastric Cancer Cells

The Anti-Cancer Effect of COX-2 Inhibitors on Gastric Cancer Cells

2007 ◽  
Vol 52 (7) ◽  
pp. 1713-1721 ◽  
Author(s):  
Soo-Jeong Cho ◽  
Nayoung Kim ◽  
Joo Sung Kim ◽  
Hyun Chae Jung ◽  
In Sung Song
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Anti Cancer ◽  
Cox 2 ◽  
Cox 2 Inhibitors

scholarly journals Tanshinone IIA Reverses the Malignant Phenotype of SGC7901 Gastric Cancer Cells

2013 ◽  
Vol 14 (1) ◽  
pp. 173-177 ◽  
Author(s):  
Min Xu ◽  
Fa-Le Cao ◽  
Nai-Yi Li ◽  
Yong-Qiang Liu ◽  
Yan-Peng Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Tanshinone Iia ◽  
Malignant Phenotype ◽  
Gastric Cancer Cells
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