Establishment of a GIST-T1 gastrointestinal stromal tumour cell line resistant to imatinib mesylate

Zhou,Yongjian; Chen,Jiabi; Weng,Xiaoyuan; Lin,Guosheng; Huang,Zicheng; Shui,Hanli

doi:10.3892/ol.2018.8283

Establishment of a GIST-T1 gastrointestinal stromal tumour cell line resistant to imatinib mesylate

Authors:
- Yongjian Zhou
- Jiabi Chen
- Xiaoyuan Weng
- Guosheng Lin
- Zicheng Huang
- Hanli Shui
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Affiliations: Department of Gastric Surgery, Union Hospital of Fujian Medical University, Fuzhou, Fujian 350001, P.R. China, Department of Urinary Surgery, The Second Hospital of Fujian Medical University, Quanzhou, Fujian 362000, P.R. China, Department of Digestive Medicine, Quanzhou First Hospital, Quanzhou, Fujian 362000, P.R. China
Published online on: March 16, 2018 https://doi.org/10.3892/ol.2018.8283
Pages: 7589-7594
Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

In the present study, imatinib mesylate (IM) was used to induce resistance in the gastrointestinal stromal tumour (GIST) cell line, GIST‑T1, to establish a stable resistant cell line. The growth characteristics and expression profile of the established cell line were compared with those of the parental cell line. Additionally, the resistance mechanism of the gastrointestinal stromal tumours was preliminarily investigated. The GIST‑T1 cells were cultured in vitro, and the drug was administered in the logarithmic phase of cell growth using intermittent dosing with increasing concentrations to obtain a drug‑resistant cell line by repeated induction. Differences in the biological behaviours of the parental cells and drug‑resistant cells were examined, and changes in the expression profiles were compared in the two cell lines. The results showed that the IM‑resistant GIST‑T1 cell line (GIST‑T1 IR) was successfully established. Analysis of the biological behaviours of the two cell lines revealed that the average doubling times of the parental cells and drug‑resistant cells were 26.59 and 33.63 h, respectively. The results of a scratch migration assay revealed that the migration ability was enhanced in the GIST‑T1 IR cells. The results of CCK‑8 detection indicated that the half maximal inhibitory concentration values of the two types of cells were 10.5 and 42.0 µM, respectively, which represented an increase of ~4‑fold in the GIST‑T1 IR cells. Flow cytometric cell cycle analysis indicated that the numbers of cells in the G0/G1, S and G2 phases increased following the induction treatment. Taken together, an IM-resistant GIST T1 cell line was successfully established, which opens novel avenues for individualized tumour chemotherapy.

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