Evaluation of Apoptotic Activity of Modified Carvacrol and Anticancer Peptide Against AGS Gastric Cancer Cell Line

Abstract IntroductionTreating stomach cancer remains a major challenge. There have been many reports of the positive effect of modified carvacrol and anti-cancer peptides on gastric cancer. The main purpose of this study was to determine and design a fusion modified carvacrol and anti-cancer peptide against AGS gastric cancer cell line using flowcytometry technique.MethodDetermination of cell lethality was conducted with different concentrations of the modified carvacrol and anti-cancer peptides against AGS cell line by MTT technique. Treatment of AGS cells with different concentrations of components to evaluate the apoptosis of AGS cells was performed by flow cytometry. In this study used. The MTT test performed according to protocol with different concentrations of components.ResultsThe results showed that the percentage of cells treated with modified carvacrol and anti-cancer peptides at a concentration of 80μg/ml with total apoptosis was 46.91% and increased by 36.25% compared to untreated cells.ConclusionDue to the anticancer properties of modified carvacrol with anticancer peptide, the above combination can be used to treat and induction apoptotic activity against gastric cancer cell line.

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Antibacterial and anti-cancer activities of Artemisia turcomanica extract on gastric cancer cell line (AGS) and its interaction on cyclin D1 and cyckin E genes

Journal of Medicinal Plants ◽

10.29252/jmp.19.74.163 ◽

2020 ◽

Vol 19 (74) ◽

pp. 163-176

Author(s):

Nooshin Fathi ◽

Farzaneh Tafvizi ◽

Amir Mirzaie ◽

◽

...

Keyword(s):

Gastric Cancer ◽

Cyclin D1 ◽

Cell Line ◽

Cancer Cell ◽

Gastric Cancer Cell ◽

Gastric Cancer Cell Line ◽

Cancer Cell Line ◽

Anti Cancer

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Anti-cancer effects of malvidin-3,5-diglucoside from Alcea longipedicellata, on gastric cancer cell line (AGS)

Planta Medica ◽

10.1055/s-0028-1084172 ◽

2008 ◽

Vol 74 (09) ◽

Author(s):

YY Kamrani ◽

B Esmaeelian ◽

M Jabbari ◽

B Tabaraei ◽

A Yazdanyar ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Line ◽

Cancer Cell ◽

Gastric Cancer Cell ◽

Gastric Cancer Cell Line ◽

Cancer Cell Line ◽

Anti Cancer

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Cytotoxic Activity of Epigallocatechin and Trans-Cinnamaldehydein Gastric Cancer Cell Line

Asian Pacific Journal of Cancer Biology ◽

10.31557/apjcb.2019.4.4.71-74 ◽

2019 ◽

Vol 4 (4) ◽

pp. 71-74

Author(s):

Attabak Toofani Milani ◽

Siamak Rashidi ◽

Reza Mahmoudi ◽

Bahareh Karimi Douna

Keyword(s):

Gastric Cancer ◽

Cell Line ◽

Cancer Cell ◽

Gastric Cancer Cell ◽

Gastric Cancer Cell Line ◽

Cancer Cell Line ◽

Cellular Viability ◽

Tumor Cell Death ◽

Ags Cells ◽

Dose Dependent

Introduction: Herbal medication is currently being utilized for treatment of numerous diseases, such as cancer which showed successful therapeutic efficacy in numerous studies. Epigallocatechin gallate (EGCG) is a compound of green tea that its role in tumor cell death has been reported. Likewise, trans-cinnamaldehyde (TC), the active ingredient in cinnamon oil showed anti-cancer properties in some previous studies. The aim of this study was to evaluate the cytotoxic effects of EGCC and TC on proliferation of gastric cancer cell line (AGS).Methods: AGS Cells were seeded and treated with various concentrations of EGCG and TC for 72 h and assessed for cell viability. To study the cytotoxic effect of drug in combination cases the lower doses than IC50 of EGCG and TC was utilized. The one-way analysis of variance (ANOVA) were used for statistical analysis.Results: various concentrations of EGCG and TC significantly inhibited the proliferation of AGS cells in dose dependent pattern. We found that in double combined cases cellular viability decreased in compared to IC50 of each single agents. Also, there were significant decrease in cellular viability in all single and double treated cases toward untreated cells (p<0.05).Conclusion: The results of this study indicated that EGCG and TC effects on AGS cell line were significantly high and dose-dependent and might be cooperative. Double combinations of these two agents may be considered as a potential therapeutic option for gastriccancer. Further investigation should be conducted to validate these combination in gastric cancer therapy.

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Enhanced Vasculogenic Capacity Induced by 5-Fluorouracil Chemoresistance in a Gastric Cancer Cell Line

International Journal of Molecular Sciences ◽

10.3390/ijms22147698 ◽

2021 ◽

Vol 22 (14) ◽

pp. 7698

Author(s):

Sara Peri ◽

Alessio Biagioni ◽

Giampaolo Versienti ◽

Elena Andreucci ◽

Fabio Staderini ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Cell Line ◽

Cancer Cell ◽

Intracellular Signaling ◽

Gastric Cancer Cell ◽

Gastric Cancer Cell Line ◽

Cancer Cell Line ◽

Tumor Evolution ◽

Selective Growth Advantage

Chemotherapy is still widely used as a coadjutant in gastric cancer when surgery is not possible or in presence of metastasis. During tumor evolution, gatekeeper mutations provide a selective growth advantage to a subpopulation of cancer cells that become resistant to chemotherapy. When this phenomenon happens, patients experience tumor recurrence and treatment failure. Even if many chemoresistance mechanisms are known, such as expression of ATP-binding cassette (ABC) transporters, aldehyde dehydrogenase (ALDH1) activity and activation of peculiar intracellular signaling pathways, a common and universal marker for chemoresistant cancer cells has not been identified yet. In this study we subjected the gastric cancer cell line AGS to chronic exposure of 5-fluorouracil, cisplatin or paclitaxel, thus selecting cell subpopulations showing resistance to the different drugs. Such cells showed biological changes; among them, we observed that the acquired chemoresistance to 5-fluorouracil induced an endothelial-like phenotype and increased the capacity to form vessel-like structures. We identified the upregulation of thymidine phosphorylase (TYMP), which is one of the most commonly reported mutated genes leading to 5-fluorouracil resistance, as the cause of such enhanced vasculogenic ability.

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