Pulsed Magnetic Fields Cause hes1 and hsa-Circ-0068530 Expression Changes in Gastric Cancer Cell Line and Human Normal Fibroblast Cell Line

Background: In recent years, the relationship between cancer cells and electromagnetic radiation has received much attention. Objectives: The present study aimed to evaluate the effects of different intensities of electromagnetic fields on gastric cancer cell lines (AGS). Methods: After preparing AGS and Hu02 (normal) cell lines, they were exposed to magnetic flux densities of 0.25, 0.5, 1, and 2 millitesla (mT) for 18 h. The cell viability was studied by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression levels of hes1 and hsa-circ-0068530 RNAs were studied by the quantitative Real-time-PCR technique. Results: The inhibition of gastric cancer cell line growth was observed under the influence of electromagnetic fields at different intensities. However, they did not affect the viability of normal cells. A sharp increase in the expression of hes1 and hsa-circ-0068530 genes was observed in normal cells exposed to 2 mT electromagnetic fields. Conclusions: In general, it can be concluded that the effect of electromagnetic fields on gastric cancer cells depends on their intensity. Magnetic flux densities of 0.25 and 0.5 mT had anti-cancer effects and magnetic flux density of 2 mT showed carcinogenic effects.

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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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