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

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 paren...

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Autores principales: Zhou, Yongjian, Chen, Jiabi, Weng, Xiaoyuan, Lin, Guosheng, Huang, Zicheng, Shui, Hanli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5934714/
https://www.ncbi.nlm.nih.gov/pubmed/29740484
http://dx.doi.org/10.3892/ol.2018.8283
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author Zhou, Yongjian
Chen, Jiabi
Weng, Xiaoyuan
Lin, Guosheng
Huang, Zicheng
Shui, Hanli
author_facet Zhou, Yongjian
Chen, Jiabi
Weng, Xiaoyuan
Lin, Guosheng
Huang, Zicheng
Shui, Hanli
author_sort Zhou, Yongjian
collection PubMed
description 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 G(0)/G(1), S and G(2) 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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spelling pubmed-59347142018-05-08 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 Oncol Lett Articles 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 G(0)/G(1), S and G(2) 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. D.A. Spandidos 2018-05 2018-03-16 /pmc/articles/PMC5934714/ /pubmed/29740484 http://dx.doi.org/10.3892/ol.2018.8283 Text en Copyright: © Zhou et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Zhou, Yongjian
Chen, Jiabi
Weng, Xiaoyuan
Lin, Guosheng
Huang, Zicheng
Shui, Hanli
Establishment of a GIST-T1 gastrointestinal stromal tumour cell line resistant to imatinib mesylate
title Establishment of a GIST-T1 gastrointestinal stromal tumour cell line resistant to imatinib mesylate
title_full Establishment of a GIST-T1 gastrointestinal stromal tumour cell line resistant to imatinib mesylate
title_fullStr Establishment of a GIST-T1 gastrointestinal stromal tumour cell line resistant to imatinib mesylate
title_full_unstemmed Establishment of a GIST-T1 gastrointestinal stromal tumour cell line resistant to imatinib mesylate
title_short Establishment of a GIST-T1 gastrointestinal stromal tumour cell line resistant to imatinib mesylate
title_sort establishment of a gist-t1 gastrointestinal stromal tumour cell line resistant to imatinib mesylate
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5934714/
https://www.ncbi.nlm.nih.gov/pubmed/29740484
http://dx.doi.org/10.3892/ol.2018.8283
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