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Effect of anticancer drugs on breast cancer cells sensitive and resistant to doxorubicin: expression of mRNAs of TGF-β and its receptors
Aim. Comparative study of the effect of chemotherapeutic drugs (doxorubicin, methotrexate and cisplatin) and TGF-β on the human breast carcinoma MCF-7 cells, sensitive (wt) and resistant (DOX/R) to the doxorubicin action. Methods. Semi-quantitative reverse transcriptase-polymerase chain reaction (RT...
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Published in: | Biopolimery i kletka 2015, Vol.30 (1), p.54-60 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | Aim. Comparative study of the effect of chemotherapeutic drugs (doxorubicin, methotrexate and cisplatin) and TGF-β on the human breast carcinoma MCF-7 cells, sensitive (wt) and resistant (DOX/R) to the doxorubicin action. Methods. Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was used for the estimation of expression of mRNAs coding for the TGF-β isoforms (TGF-β1 and TGF-β2) and the TGF-β type I and II receptors (TRI and TRII). Trypan blue exclusion method was used for measuring cell number and cell viability. Results. The MCF-7(DOX/R) cells were more refractory to the TGF1-dependent growth inhibition than the MCF-7(wt) cells. The level of mRNAs coding for TGF and its receptors was higher in the untreated MCF-7 (DOX/R) cells comparing to the MCF-7(wt) cells. The expression of mRNA coding for TRII was decreased in both cell lines treated with doxorubicin, methotrexate and cisplatin, while the down-regulation of mRNA coding for TRI was revealed only in the MCF-7(DOX/R) cells upon the treatment with doxorubicin and methotrexate. Conclusions. The differential effects of studied anticancer drugs and TGF-β on the doxorubicin-sensitive and -resistant cells have been demonstrated. The elucidation of the molecular mechanisms of escape of the MCF-7 (DOX/R) cells from the growth inhibition by TGF-β requires further investigation. |
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ISSN: | 0233-7657 1993-6842 |
DOI: | 10.7124/bc.00087E |