Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin

Heat shock protein 27 (Hsp27) and Hsp70 have been involved in resistance to anticancer drugs in human breast cancer cells growing in vitro and in vivo. In this study, we examined the expression of Hsp25 (the rodent homologue to human Hsp27) and Hsp70 in 3 different rodent tumors (a mouse breast carc...

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Autores principales: Ciocca, Daniel R., Rozados, Viviana R., Cuello Carrión, F. Darío, Gervasoni, Silvia I., Matar, Pablo, Scharovsky, O. Graciela
Formato: article artículo publishedVersion
Lenguaje:Inglés
Publicado: Springer 2012
Acceso en línea:http://hdl.handle.net/2133/1935
http://hdl.handle.net/2133/1935
Aporte de:
Repositorio Hipermedial de la Universidad Nacional de Rosario (UNR) de Universidad Nacional de Rosario
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institution Universidad Nacional de Rosario
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repository_str R-121
collection Repositorio Hipermedial de la Universidad Nacional de Rosario (UNR)
language Inglés
orig_language_str_mv en
description Heat shock protein 27 (Hsp27) and Hsp70 have been involved in resistance to anticancer drugs in human breast cancer cells growing in vitro and in vivo. In this study, we examined the expression of Hsp25 (the rodent homologue to human Hsp27) and Hsp70 in 3 different rodent tumors (a mouse breast carcinoma, a rat sarcoma, and a rat lymphoma maintained by subcutaneous passages) treated in vivo with doxorubicin (DOX) and lovastatin (LOV). All tumors showed massive cell death under control untreated conditions, and this massive death increased after cytotoxic drug administration. In this study, we show that this death was due to classic apoptosis. The tumors also showed isolated apoptotic cells between viable tumor cells, and this occurred more significantly in the lymphoma. The tumor type that was more resistant to cell death was the sarcoma, and this was found in sarcomas growing both under control conditions and after cytotoxic drug administration. Moreover, sarcomas showed the highest expression levels of Hsp25 in the viable tumor cells growing under untreated conditions, and these levels increased after DOX and LOV administration. After drug treatment, only sarcoma tumor cells showed a significant increase in Hsp70. In other words, sarcomas were the tumors with lower cell death, displayed a competent Hsp70 and Hsp25 response with nuclear translocation, and had the highest levels of Hsp25. In sarcomas, Hsp25 and Hsp70 were found in viable tumor cells located around the blood vessels, and these areas showed the most resistant tumor cell phenotype after chemotherapy. In addition, Hsp25 expression was found in endothelial cells as unique feature revealed only in lymphomas. In conclusion, our study shows that each tumor type has unique features regarding the expression of Hsp25 and Hsp70 and that these proteins seem to be implicated in drug resistance mainly in sarcomas, making these model systems important to perform more mechanistic studies on the role of Hsps in resistance to certain cytotoxic drugs.
format article
artículo
publishedVersion
author Ciocca, Daniel R.
Rozados, Viviana R.
Cuello Carrión, F. Darío
Gervasoni, Silvia I.
Matar, Pablo
Scharovsky, O. Graciela
spellingShingle Ciocca, Daniel R.
Rozados, Viviana R.
Cuello Carrión, F. Darío
Gervasoni, Silvia I.
Matar, Pablo
Scharovsky, O. Graciela
Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin
author_facet Ciocca, Daniel R.
Rozados, Viviana R.
Cuello Carrión, F. Darío
Gervasoni, Silvia I.
Matar, Pablo
Scharovsky, O. Graciela
author_sort Ciocca, Daniel R.
title Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin
title_short Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin
title_full Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin
title_fullStr Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin
title_full_unstemmed Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin
title_sort hsp25 and hsp70 in rodent tumors treated with doxorubicin and lovastatin
publisher Springer
publishDate 2012
url http://hdl.handle.net/2133/1935
http://hdl.handle.net/2133/1935
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