Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA119425 | ENA |
REPOSITORIES: ENA
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Project description:Trifluorothymidine (TFT) is part of the novel oral formulation TAS-102, which is currently evaluated in phase II studies. Drug resistance is an important limitation of cancer therapy. The aim of the present study was to induce resistance in the colon cancer cell line H630 using two different exposure schedules and to analyze the resistance mechanism. Cells were exposed either continuously or intermittently to TFT, resulting in H630-cTFT and H630-4TFT, respectively. Cells were analyzed for cross resistance, cell cycle, protein expression and activity of thymidine phosphorylase (TP), thymidine kinase (TK) and thymidylate synthase (TS), gene expression (microarray) and genomic alterations (array CGH). Both cell lines were cross-resistant to 2’-deoxy-5-fluorouridine (>170-fold). Exposure to IC75-TFT increased the S- and G2/M-phase of H630 cells, while in the resistant variants no change was observed. The two main target enzymes TS and TP remained unchanged in both TFT-resistant variants. In H630-4TFT cells, TK protein expression and activity were decreased, possibly related to an aberrant TK protein, clearly resulting in less activated TFT and most likely the mechanism of TFT resistance. Surprisingly, in H630-cTFT microarray analysis revealed a strong increase in mRNA levels of secretory phospholipase-A2 (sPLA2; 47-fold), which was also found by RT-PCR (211 fold increase). Inhibition of sPLA2 reversed TFT resistance partially. In addition, H630-cTFT had many chromosomal aberrations, but the exact role of sPLA2 in TFT-resistance remains unclear. Altogether, induction of resistance to TFT can lead to different mechanisms of resistance, including decreased TK protein expression and enzyme activity, as well as (phospho)lipid metabolism.
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