Autor: |
Rhodes LV; Department of Medicine, Section of Hematology and Medical Oncology, Tulane University Health Sciences Center, New Orleans, LA 70112, USA., Nitschke AM, Segar HC, Martin EC, Driver JL, Elliott S, Nam SY, Li M, Nephew KP, Burow ME, Collins-Burow BM |
Jazyk: |
angličtina |
Zdroj: |
Oncology reports [Oncol Rep] 2012 Jan; Vol. 27 (1), pp. 10-6. Date of Electronic Publication: 2011 Oct 04. |
DOI: |
10.3892/or.2011.1488 |
Abstrakt: |
The development of drug resistance represents a major complication in the effective treatment of breast cancer. Epigenetic therapy, through the use of histone deacetylase inhibitors (HDACi) or demethylation agents, is an emerging area of therapeutic targeting in a number of ontological entities, particularly in the setting of aggressive therapy-resistant disease. Using the well-described HDAC inhibitor trichostatin A (TSA) we demonstrate the suppression of in vitro clonogenicity in the previously described apoptosis-resistant MCF-7TN-R breast carcinoma cell line. Additionally, recent work has demonstrated that these agents can alter the expression profile of microRNA signatures in malignant cells. Using an unbiased microRNA microarray analysis, changes in miRNA expression of MCF-7TN-R cells treated with TSA for 24 h were analyzed. We observed significant up-regulation of 22 miRNAs and down-regulation of 10 miRNAs in response to TSA treatment. Our results demonstrate that the HDACi, TSA, exerts anticancer activity in the apoptosis-resistant MCF-7TN-R breast carcinoma cell line. This activity is correlated with TSA alteration of microRNA expression profiles indicative of a less aggressive phenotype. |
Databáze: |
MEDLINE |
Externí odkaz: |
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