Characteristics of five human tumor cell lines and sublines resistant to cis‐diamminedichloroplatinum(II)

Teicher, Beverly A.; Holden, Sylvia A.; Herman, Terence S.; Sotomayor, Enrique Alvarez; Khandekar, Vrinda S.; Rosbe, Kristina W.; Brann, Terrence W.; Korbut, Timothy T.; Frei, Emil

doi:10.1002/ijc.2910470214

Cited by 125 publications

(93 citation statements)

References 36 publications

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“…However, the deletion of S-1-P lyase-, RegA-and PIP5K-encoding genes did not result in resistance to other DNAdamaging agents in addition to cisplatin. The specificity for resistance to cisplatin in Dictyostelium is similar to that observed with several cisplatin-resistant tumour cell lines (Teicher et al, 1991 ;Rabo et al, 1996) and is important because it offers specific potential target pathways for chemotherapeutic agents.…”

Section: Discussionsupporting

confidence: 57%

Molecular basis for resistance to the anticancer drug cisplatin in Dictyostelium The GenBank accession numbers for the sequences reported in this paper are AF233610 (S-1-P lyase), AF233612 (PIP5K), AF233611 (P2Y purine receptor 1), AF233613 (CAAX prenyl protease) and AF233614 (unidentified gene).

Alexander

Schneider

et al. 2000

Microbiology

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The efficacy of the widely used chemotherapeutic drug cisplatin is limited by the occurrence of drug-resistant tumour cells. To fully exploit the potential of this drug in cancer therapy, it is imperative to understand the molecular basis of cisplatin resistance. Using an insertional mutagenesis technique in cells of Dictyostelium discoideum, we have identified six genes which are involved in cisplatin resistance. None of these genes has been previously linked to resistance to this drug. Several of these genes encode proteins that are involved in signal transduction pathways which regulate cell death, cell proliferation or gene regulation. The resistance of these mutant strains is specific for cisplatin, since deletion of these genes does not confer resistance to other DNA-damaging agents. Significantly, the disruption of three of these genes, encoding the sphingosine-1-phosphate lyase, the RegA cAMP phosphodiesterase and a phosphatidylinositol-4-phosphate 5-kinase, also results in abnormalities in the multicellular development of this organism, although there is no change in the rate of mitotic cell growth. This study has identified previously unsuspected molecular pathways which function in the cellular response to cisplatin and are required for normal morphogenesis, and underscores the complexity of the cellular response to cisplatin. These pathways provide potential targets for modulating the response to this important drug.

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Section: Discussionsupporting

confidence: 57%

Molecular basis for resistance to the anticancer drug cisplatin in Dictyostelium The GenBank accession numbers for the sequences reported in this paper are AF233610 (S-1-P lyase), AF233612 (PIP5K), AF233611 (P2Y purine receptor 1), AF233613 (CAAX prenyl protease) and AF233614 (unidentified gene).

Alexander

Schneider

et al. 2000

Microbiology

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“…Teicher et al (21) developed a cw-platinum-resistant head and neck squamous cell carcinoma cell line which, among other changes, displayed an increased GST activity. Numerous cell lines selected for resistance towards common chemothera peutic drugs over-express GSTs.…”

Section: Discussionmentioning

confidence: 99%

Glutathione S-transferases and glutathione in human head and neck cancer

Mulder¹,

Manni

Roelofs³

et al. 1995

Carcinogenesis

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Glutathione S-transferase (GST) enzyme activity, GST isoenzyme composition and glutathione (GSH) concentra tion were assessed in normal and squamous cell carcinoma specimens of 14 patients with oral or oropharyngeal cancer and 11 patients with laryngeal cancer. Comparing malig nant with normal oral/oropharyngeal tissues, no significant differences in GSH content, GST enzyme activity or iso enzyme composition were found. However, some tumours had up to 3-fold increased GST enzyme activities and 11 malignant samples over-expressed GST-tc. GST-tc was present in all normal and malignant oral/oropharyngeal specimens investigated, whereas class a and class \i were detected in only a few samples. GST-fj. was present in 28% of the patients with oral/oropharyngeal tumours as compared with -60% in the normal population. GST-a, -|i and -71 were detected in 91, 64 and 100% of the normal laryngeal tissues respectively. In laryngeal tumours signi ficantly higher levels of GST-tc and GSH but signi ficantly lower amounts of GST-a were detected. Levels of class p GST were generally lower in cancerous tissues, but differences were not significant. In comparison with normal oral/oropharyngeal tissues, normal laryngeal tissues con tained almost twice the amount of GST enzyme activity due to higher class a enzyme levels. It is concluded that (ÏST-7C is elevated in 11 out of 14 tumours of the oral cavity and values are significantly increased in tumours of the larynx, which may contribute to the inherent anti-cancer drug resistance of these malignancies. In laryngeal tumours the increased GSH levels may confer additional resistance to radiation therapy.

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“…32 We have found that the activity of GST was found increased more than 14-fold in Adr R MCF-7 cell as compared with MCF-7, consistent with previous reports of indicating the enzyme correlation with human breast cancer and other tumor cell lines undergoing drug resistance. [33][34][35][36][37][38] Glutathione contents in Adr R MCF-7 and Vin R KB cells were both increased, while Vin R KB cell did not show the same increase of GST activity.…”

Section: Discussionmentioning

confidence: 99%

Chemosensitizing multiple drug resistance of human carcinoma by bicyclol involves attenuated P-glycoprotein, GST-P and Bcl-2

Zhu

Liu²,

Zhao³

et al. 2006

Cancer Biology & Therapy

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Bicyclol, a second generation of synthetic hepatoprotectant being used in China for anti-hepatitis therapy, shows chemosensitizing effect on reverting multiple drug resistance (MDR) of cytostatic agents in two established MDR carcinoma cell lines, vincristine resistant human stomatic epidermoid carcinoma Vin R KB and adriamycin resistant human breast carcinoma Adr R MCF-7. The reversal rate of drug resistance was calculated from the changes of the IC 50 of cell growth inhibition. Bicyclol at the concentration of 25, 50, 100 µM induced 2.8 7.3 and 20.7 fold, respectively, reversal of vincristine resistance in Vin R KB cell. Bicyclol also reversed the cross-resistance of Vin R KB cell to taxol and Adr R MCF-7 cell resistance to adriamycin at the similar range of potency. Further, Bicyclol recovered the reduced accumulation of adriamycin in Adr R MCF-7 cell partially to the level in drugsensitive MCF-7 cell, indicate the inhibition of MDR related membrane efflux pump system. Overexpression of membrane p-glycoprotein coded by Mdr-1 genes, the most common efflux pump correlated to MDR, was found in both Vin R KB and Adr R MCF-7 cells by Western blot and immunocytochemistry as compared with drug-sensitive cells. The p-glycoprotein was decreased to the levels in drug-sensitive cells when Vin R KB and Adr R MCF-7 cells were treated with Bicyclol for 12-72 hours. Both Vin R KB and Adr R MCF-7 cells showed increased GSH contents, and Adr R MCF-7 cell showed increased GST activity and the overexpression of Bcl-2 protein, by which molecules are tightly related to the MDR formation besides Mdr-1 p-glycoprotein. Bicyclol reduced the GSH contents, GST activities and Bcl-2 expression. All these data demonstrate that, by modifying the expressions of Mdr-1, GSH/GST and Bcl-2, Bicyclol increases the intracellular drug concentration and sensitizes the resistant cells to the anti-carcinoma agents.

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Characteristics of five human tumor cell lines and sublines resistant to cis‐diamminedichloroplatinum(II)

Cited by 125 publications

References 36 publications

Molecular basis for resistance to the anticancer drug cisplatin in Dictyostelium The GenBank accession numbers for the sequences reported in this paper are AF233610 (S-1-P lyase), AF233612 (PIP5K), AF233611 (P2Y purine receptor 1), AF233613 (CAAX prenyl protease) and AF233614 (unidentified gene).

Molecular basis for resistance to the anticancer drug cisplatin in Dictyostelium The GenBank accession numbers for the sequences reported in this paper are AF233610 (S-1-P lyase), AF233612 (PIP5K), AF233611 (P2Y purine receptor 1), AF233613 (CAAX prenyl protease) and AF233614 (unidentified gene).

Glutathione S-transferases and glutathione in human head and neck cancer

Chemosensitizing multiple drug resistance of human carcinoma by bicyclol involves attenuated P-glycoprotein, GST-P and Bcl-2

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