Ocimum Gratissimum Extract Induces Apoptosis in Gastric Cancer Cells via Modulation of Reactive Oxygen Species and Mitogen-Activated Protein Kinase

2020 ◽  
Vol 19 (4) ◽  
pp. 514-519
Author(s):  
Ming-Jen Sheu ◽  
Jen-Ning Tsai ◽  
Wai-Lun Tam ◽  
Jer-Yuh Liu ◽  
Li-Sung Hsu
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Mitogen Activated Protein Kinase ◽  
High Rate ◽  
Anticancer Activities ◽  
Gastric Cancer Cells ◽  
Cancer Proliferation ◽  
Ocimum Gratissimum ◽  
Cancer Agent

Given the increasing incidence of gastric cancer and its high rate of metastasis, drug resistance and the mortality rate remain high. Ocimum gratissimum, a botanical species of Ocimum known to exhibit general anti-inflammatory, antioxidant, and anticancer activities has not yet been evaluated for gastric cancer proliferation. In this study, we have demonstrated that O. gratissimum extract significantly reduces the viability of gastric cancer cells by triggering apoptosis, elevating levels of ROS, and enhanced cleavage of poly-ADP-ribose polymerase and caspase-3. Western blot analysis indicated that O. gratissimum extract enhanced the cleavage of PARP and caspase-3. Moreover, O. gratissimum extract inhibited extracellular signal-regulated kinase 1/2 and increased activities of p38, a stress stimulated kinase. In conclusion, our findings show that O. gratissimum extract may be a potential antigastric cancer agent.

Light activation of cyclometalated ruthenium complexes drives towards caspase 3 dependent apoptosis in gastric cancer cells

2020 ◽  
Vol 208 ◽  
pp. 111080 ◽  
Author(s):  
Jorge Andrés Solís-Ruiz ◽  
Anaïs Barthe ◽  
Gilles Riegel ◽  
Rafael Omar Saavedra-Díaz ◽  
Christian Gaiddon ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Ruthenium Complexes ◽  
Light Activation ◽  
Gastric Cancer Cells

scholarly journals Arsenic trioxide induces apoptosis in human gastric cancer cells through up-regulation of p53 and activation of caspase-3

2001 ◽  
Vol 93 (6) ◽  
pp. 916-916 ◽  
Author(s):  
XH Jiang ◽  
BCY Wong ◽  
ST Yuen ◽  
SH Jiang ◽  
CH Cho ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Caspase 3 ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

Babao dan promotes apoptosis of cisplatin (DDP)-resistant gastric cancer cell line SGC-7901/DDP by inducing autophagy through PI3K/AKT/mTOR pathway modulation

2020 ◽  
Author(s):  
Jinyan Zhao ◽  
Weilan Lan ◽  
Jun Peng ◽  
Bin Guan ◽  
Jie Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Cell Line ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Mtor Pathway ◽  
Cell Protein ◽  
Drug Resistant ◽  
Gastric Cancer Cells

Abstract Background: Multidrug resistance (MDR) is a critical reason of cancer chemotherapy failure. Babao dan (BBD) is a classical and famous traditional Chinese patent medicine, which has been reported to has anti-gastric cancer activity. However, the roles and molecular mechanisms of the reversal of MDR of gastric cancer by BBD have not been well described until now. Methods: SGC-7901 and SGC-7901/DDP cells were used in this study, and drug resistance and evaluation of the reversal effect of BBD was determined using MTT assays in SGC7901/DDP cells. Doxorubicin (DOX) and Rhodamin123 (Rho123) staining was performed to assess BBD effects on drug accumulation and efflux of drug-resistant gastric cancer cells. Cell apoptosis was directly assessed using DAPI staining. Apoptotic and dead cells were detected by flow cytometry after staining with Annexin V-FITC and propidium iodide (PI). Cyto-ID assays were performed to examine cellular autophagy. Changes in cell protein expression of ABCB1, ABCC1, ABCG2, Bax, Bcl-2, caspase-3, cleaved-caspase-3, LC3, p62, Beclin1 and the PI3K/AKT/mTOR pathway were detected by Western blot. Inhibition of autophagy with 3-MA, chloroquine (CQ) and PI3K antagonist (LY294002) or agonist (740Y-P) , uncovered a role for the potentially downregulated signaling pathway, PI3K/AKT/mTOR.Results: The SGC7901/DDP cell line exhibited multi-drug resistance to DDP, DOX and 5-fluorouracil (5-FU) and the drug resistant index (RI) of DDP, DOX and 5-FU were 1.86, 1.50 and 47.70, respectively. BBD reversed the MDR of SGC7901/DDP cells by increasingDOX accumulation, reducing Rh123 efflux and down-regulating the expression of ABCB1, ABCC1, ABCG2. Furthermore, BBD induced apoptosis in SGC7901/DDP cells through regulating caspase-3, cleaved-caspase-3, Bax and Bcl-2. Moreover, BBD induced autophagy in DDP-resistant gastric cancer cells via regulating p62, LC3 and Beclin1. Pathway analyses suggested BBD may inhibit PI3K/AKT/mTOR pathway activity and subsequent autophagy induction. Conclusions: BBD may reverse the MDR of gastric cancer cells, and promote autophagic death via inactivation of the PI3K/AKT/mTOR signaling pathway.

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.

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