We are analyzing https://link.springer.com/article/10.1007/s002800100294.

Title:
Antineoplastic action of 5-aza-2′-deoxycytidine and histone deacetylase inhibitor and their effect on the expression of retinoic acid receptor β and estrogen receptor α genes in breast carcinoma cells | Cancer Chemotherapy and Pharmacology
Description:
Purpose: During tumorigenesis several cancer-related genes can be silenced by aberrant methylation. In many cases these silenced genes can be reactivated by exposure to the DNA methylation inhibitor, 5-aza-2′-deoxycytidine (5-AZA-CdR). Histone acetylation also plays a role in the control of expression of some genes. The aim of this study was to determine the antineoplastic activities of 5-AZA-CdR and trichostatin A (TSA), either administered alone or in combination, in MDA-MB-231 breast carcinoma cells. The effects of these drugs (alone and in combination) on the expression of the tumor suppressor gene, retinoic acid receptor (RARβ) and of the estrogen receptor α gene (ERα), whose expression is lost in the cell line used in the study, were also investigated. Methods: MDA-MB-231 cells were treated with 5-AZA-CdR and TSA and the antitumor activity of these drugs was determined by clonogenic assay. Total RNA was extracted from the treated cells and RT-PCR was used to determine the effect of the treatment on the expression of RARβ and ERα. Methylation-sensitive PCR analysis was used to confirm that lack of expression of both genes was due to hypermethylation of their promoter regions. A single nucleotide primer extension assay was also used to quantify the reduction in DNA methylation following drug treatment. Results: Both 5-AZA-CdR and TSA alone showed significant antineoplastic activity. The combination of the two drugs was synergistic with respect to MDA-MB-231 cell kill. 5-AZA-CdR alone weakly activated the expression of both RARβ and ERα. TSA alone only activated RARβ, but not ERα. The combination of these agents appeared to produce a greater activation of both genes. Conclusions: The interesting interaction between 5-AZA-CdR and TSA in both cell kill and cancer-related gene reactivation provides a rationale for the use of inhibitors of DNA methylation and histone deacetylation in combination for the chemotherapy of breast cancer.
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Keywords {🔍}

article, receptor, cancer, expression, breast, methylation, genes, cells, azacdr, access, privacy, cookies, content, estrogen, dna, tsa, combination, information, publish, search, antineoplastic, azadeoxycytidine, histone, retinoic, acid, rarβ, erα, analysis, data, log, journal, research, chemotherapy, inhibitor, effect, carcinoma, july, bovenzi, momparler, mdamb, drugs, gene, cell, treatment, open, discover, springer, optional, personal, parties,

Topics {✒️}

methylation-sensitive pcr analysis month download article/chapter cancer-related gene reactivation estrogen-independent aggressive phenotype dna methylation inhibitor retinoic acid receptor tumor suppressor gene breast carcinoma cells mda-mb-231 cell kill dna methylation article cancer chemotherapy estrogen receptor alpha cancer-related genes mda-mb-231 cells related subjects privacy choices/manage cookies full article pdf breast cancer drug treatment université de montréal aberrant methylation article bovenzi european economic area july 2001 volume 48 chronic oxidative stress hôpital ste-justine 3175 côte ste-catherine conditions privacy policy usage analysis check access instant access histone deacetylase inhibitor accepting optional cookies québec h3t 1c5 main content log journal finder publish article log epigenetic inactivation article cite antineoplastic action treated cells privacy policy personal data cell kill information clonogenic assay books a 5-aza-2′-deoxycytidine optional cookies manage preferences

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         description: Purpose: During tumorigenesis several cancer-related genes can be silenced by aberrant methylation. In many cases these silenced genes can be reactivated by exposure to the DNA methylation inhibitor, 5-aza-2′-deoxycytidine (5-AZA-CdR). Histone acetylation also plays a role in the control of expression of some genes. The aim of this study was to determine the antineoplastic activities of 5-AZA-CdR and trichostatin A (TSA), either administered alone or in combination, in MDA-MB-231 breast carcinoma cells. The effects of these drugs (alone and in combination) on the expression of the tumor suppressor gene, retinoic acid receptor (RARβ) and of the estrogen receptor α gene (ERα), whose expression is lost in the cell line used in the study, were also investigated. Methods: MDA-MB-231 cells were treated with 5-AZA-CdR and TSA and the antitumor activity of these drugs was determined by clonogenic assay. Total RNA was extracted from the treated cells and RT-PCR was used to determine the effect of the treatment on the expression of RARβ and ERα. Methylation-sensitive PCR analysis was used to confirm that lack of expression of both genes was due to hypermethylation of their promoter regions. A single nucleotide primer extension assay was also used to quantify the reduction in DNA methylation following drug treatment. Results: Both 5-AZA-CdR and TSA alone showed significant antineoplastic activity. The combination of the two drugs was synergistic with respect to MDA-MB-231 cell kill. 5-AZA-CdR alone weakly activated the expression of both RARβ and ERα. TSA alone only activated RARβ, but not ERα. The combination of these agents appeared to produce a greater activation of both genes. Conclusions: The interesting interaction between 5-AZA-CdR and TSA in both cell kill and cancer-related gene reactivation provides a rationale for the use of inhibitors of DNA methylation and histone deacetylation in combination for the chemotherapy of breast cancer.
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      headline:Antineoplastic action of 5-aza-2′-deoxycytidine and histone deacetylase inhibitor and their effect on the expression of retinoic acid receptor β and estrogen receptor α genes in breast carcinoma cells
      description: Purpose: During tumorigenesis several cancer-related genes can be silenced by aberrant methylation. In many cases these silenced genes can be reactivated by exposure to the DNA methylation inhibitor, 5-aza-2′-deoxycytidine (5-AZA-CdR). Histone acetylation also plays a role in the control of expression of some genes. The aim of this study was to determine the antineoplastic activities of 5-AZA-CdR and trichostatin A (TSA), either administered alone or in combination, in MDA-MB-231 breast carcinoma cells. The effects of these drugs (alone and in combination) on the expression of the tumor suppressor gene, retinoic acid receptor (RARβ) and of the estrogen receptor α gene (ERα), whose expression is lost in the cell line used in the study, were also investigated. Methods: MDA-MB-231 cells were treated with 5-AZA-CdR and TSA and the antitumor activity of these drugs was determined by clonogenic assay. Total RNA was extracted from the treated cells and RT-PCR was used to determine the effect of the treatment on the expression of RARβ and ERα. Methylation-sensitive PCR analysis was used to confirm that lack of expression of both genes was due to hypermethylation of their promoter regions. A single nucleotide primer extension assay was also used to quantify the reduction in DNA methylation following drug treatment. Results: Both 5-AZA-CdR and TSA alone showed significant antineoplastic activity. The combination of the two drugs was synergistic with respect to MDA-MB-231 cell kill. 5-AZA-CdR alone weakly activated the expression of both RARβ and ERα. TSA alone only activated RARβ, but not ERα. The combination of these agents appeared to produce a greater activation of both genes. Conclusions: The interesting interaction between 5-AZA-CdR and TSA in both cell kill and cancer-related gene reactivation provides a rationale for the use of inhibitors of DNA methylation and histone deacetylation in combination for the chemotherapy of breast cancer.
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      dateModified:
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         Oncology
         Pharmacology/Toxicology
         Cancer Research
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