scholarly journals Insulin-like growth factor-I induces epithelial to mesenchymal transition via GSK-3β and ZEB2 in the BGC-823 gastric cancer cell line

2014 ◽  
Vol 9 (1) ◽  
pp. 143-148 ◽  
Author(s):  
HEMING LI ◽  
LING XU ◽  
LEI ZHAO ◽  
YANJU MA ◽  
ZHITU ZHU ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Growth Factor ◽  
Cell Line ◽  
Gastric Cancer Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Gastric Cancer Cell Line ◽  
Cancer Cell Line ◽  
Mesenchymal Transition ◽  
Factor I ◽  
Gsk 3Β

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

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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