Ultrastructural morphology and localisation of cisplatin-induced platinum–DNA adducts in a cisplatin-sensitive and -resistant human small cell lung cancer cell line using electron microscopy

Meijera, Coby; Luyn, Marja J. A. van; Nienhuis, Edith F.; Blom, Nel R.; Mulder, Nanno; Vries, Elisabeth G.E. de

doi:10.1016/s0006-2952(00)00584-0

Cited by 31 publications

(31 citation statements)

References 10 publications

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“…Attempts to map the subcellular distribution of DDP in the cell using energy-dispersive X-ray microanalysis (43)(44)(45), electronic probes (46), or electron microscopy (47) have been hampered by the limited intracellular accumulation of the drug. Recently Molenaar et al (34) described the synthesis of a fluorescein-labeled form of DDP and reported on its use for studying the cellular pharmacology of this drug.…”

Section: Discussionmentioning

confidence: 99%

Confocal Microscopic Analysis of the Interaction between Cisplatin and the Copper Transporter ATP7B in Human Ovarian Carcinoma Cells

Katano

Safaei

Samimi

et al. 2004

Clinical Cancer Research

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Section: Discussionmentioning

confidence: 99%

Confocal Microscopic Analysis of the Interaction between Cisplatin and the Copper Transporter ATP7B in Human Ovarian Carcinoma Cells

Katano

Safaei

Samimi

et al. 2004

Clinical Cancer Research

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“…After analyzing the ultrastructural morphololgy, Meijera et al (18) found an extensive Golgi apparatus and an increased number of mitochondria in the human small cell lung cancer cisplatin-resistant cell line, GLC4-CDDP cells, in contrast to its parental cell line, GLC 4 . These changes might facilitate the cisplatin-resistant cell survival by increasing energy production/metabolism and further increasing DNA repair directly, or modulating the signal transduction pathways leading to cell death indirectly.…”

Section: Discussionmentioning

confidence: 99%

Establishment and biological analysis of the EC109/CDDP multidrug-resistant esophageal squamous cell carcinoma cell line

Wen¹,

Zheng²,

Hu³

et al. 2009

Oncol Rep

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Abstract. The aim of this study was to establish a stable, drug-resistant esophageal squamous cell carcinoma (ESCC) cell line. The human ESCC cell line EC109 was exposed to cisplatin (CDDP) by pulse treatment to select for the drugresistant subline, EC109/CDDP cells. The MTT assay was used to test the drug resistance of EC109 and EC109/CDDP cells. In addition, cellular morphological changes were observed using microscopy and the growth curves of the two cell lines were drawn to calculate the doubling time. Furthermore, cell cycle distribution was analyzed by flow cytometry. Finally, RT-PCR was performed to determine the mRNA expression levels of drug-resistant-related genes, multidrug resistance 1 (MDR1), multidrug resistanceassociated protein 1 (MRP1), ATP-binding cassette, subfamily G, member 2 (ABCG2), lung resistance protein (LRP), and glutathione S-transferase (GST)-pi in both cell lines. EC109/CDDP cells exhibited increased resistance to CDDP, carboplatin, 5-fluorouracil, taxol, navelbine, irinotecan and etoposide, and changes in morphology, doubling time, and cell cycle distribution were detected as compared with EC109 cells. Although there was no significant difference in MRP1, ABCG2, LRP, and GST-pi expression, MDR1 expression in EC109/CDDP cells was lower than that of EC109 cells. EC109/CDDP cells are a stable, multidrug-resistant ESCC cell line and could serve as an important tool for further research concerning ESCC drug resistance.

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“…1,3,4 Breast cancer cells were notably reported to develop resistance towards chemotherapy agents, including platinum derivatives such as cisplatin. [4][5][6] Until recently, the clear mechanism of drug resistance of breast cancer cell is still in debate. [4][5][6][7][8] Many studies have reported several possible mechanisms which are related to chemo-resistance, including over-expression of p-glycoprotein, alteration of cell cycle arrest and apoptosis, the expression of multidrug resistance-associated protein (MRP).…”

Section: Introductionmentioning

confidence: 99%

“…[4][5][6] Until recently, the clear mechanism of drug resistance of breast cancer cell is still in debate. [4][5][6][7][8] Many studies have reported several possible mechanisms which are related to chemo-resistance, including over-expression of p-glycoprotein, alteration of cell cycle arrest and apoptosis, the expression of multidrug resistance-associated protein (MRP). 5,6 Overall, all these molecular mechanisms will result in the drug-resistant phenotype modification, which could be accompanied by changes in proliferation potential and morphological structure.…”

Section: Introductionmentioning

confidence: 99%

“…[4][5][6][7][8] Many studies have reported several possible mechanisms which are related to chemo-resistance, including over-expression of p-glycoprotein, alteration of cell cycle arrest and apoptosis, the expression of multidrug resistance-associated protein (MRP). 5,6 Overall, all these molecular mechanisms will result in the drug-resistant phenotype modification, which could be accompanied by changes in proliferation potential and morphological structure. 5 Therefore, in order to observe the characteristics in the early stages of acquired drug-resistance in breast cancer, structure of the cell cancer might provide an initial insight of the development of chemo-resistance.…”

Section: Introductionmentioning

confidence: 99%

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Morphological Changes of Cisplatin-resistant Human Breast Cancer MCF-7 Cell Line

Puspita

Bedford

2017

IJIHS

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Objective: To evaluate morphological changes of breast cancer cell line MCF-7 following the development of acquired resistance towards cisplatin. Resistance towards anticancer agents still plays an important role in the breast cancer chemotherapy failure. Methods:The cisplatin resistant subline MCF-7/CisR was developed in-vitro by cultivating the parental cell line cisplatin-sensitive MCF-7 with raising concentration of cisplatin (from 0.01 to 2.3 µM) for four months. The cell morphology was observed by giemsa staining. Results:The resistance was shown by the increase of IC 50 by 9 folds on MCF-7/CisR compared to the initial IC 50 value of MCF-7. The change in cisplatin cytotoxic potency on the resistant cell line was accompanied by the morphological modification, including the enlargement of cell size, the increase of nucleus and cytoplasm ratio, and the increase of the number of microvesicular and cytoplasmic granules. Conclusions:This result has supported the underlying mechanism of cisplatin resistance, including the ability of the cells to decrease intracellular cisplatin concentration and repair DNA damage effects.

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Ultrastructural morphology and localisation of cisplatin-induced platinum–DNA adducts in a cisplatin-sensitive and -resistant human small cell lung cancer cell line using electron microscopy

Cited by 31 publications

References 10 publications

Confocal Microscopic Analysis of the Interaction between Cisplatin and the Copper Transporter ATP7B in Human Ovarian Carcinoma Cells

Confocal Microscopic Analysis of the Interaction between Cisplatin and the Copper Transporter ATP7B in Human Ovarian Carcinoma Cells

Establishment and biological analysis of the EC109/CDDP multidrug-resistant esophageal squamous cell carcinoma cell line

Morphological Changes of Cisplatin-resistant Human Breast Cancer MCF-7 Cell Line

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