Cancer chemoprevention by an adenosine derivative in a model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in rats

Hepatocellular carcinoma is one of the most common cancers, and approximately 80% develop from cirrhotic livers. We have previously shown that the aspartate salt of adenosine prevents and reverses carbon tetrachloride-induced liver fibrosis in rats. Considering the hepatoprotective role of this aden...

Descripción completa

Detalles Bibliográficos
Autor: JULIO ISAEL PÉREZ CARREÓN
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2017
País:México
Institución:Instituto Nacional de Medicina Genómica
Repositorio:Repositorio del Instituto Nacional de Medicina Genómica
OAI Identifier:oai:repositorio.inmegen.gob.mx:14
Acceso en línea:http://repositorio.inmegen.gob.mx/record/14
Access Level:acceso abierto
Palabra clave:info:eu-repo/classification/cti/3
id MX_4e32a96bc9ceed13a331ca2ce87d3b46
oai_identifier_str oai:repositorio.inmegen.gob.mx:14
network_acronym_str MX
network_name_str México
repository_id_str
spelling Cancer chemoprevention by an adenosine derivative in a model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in ratsJULIO ISAEL PÉREZ CARREÓNinfo:eu-repo/classification/cti/3 Hepatocellular carcinoma is one of the most common cancers, and approximately 80% develop from cirrhotic livers. We have previously shown that the aspartate salt of adenosine prevents and reverses carbon tetrachloride-induced liver fibrosis in rats. Considering the hepatoprotective role of this adenosine derivative in fibrogenesis, we were interested in evaluating its effect in a hepatocarcinogenesis model induced by diethylnitrosamine in rats, where multinodular cancer is preceded by cirrhosis. Rats were injected with diethylnitrosamine for 12 weeks to induce cirrhosis and for 16 weeks to induce hepatocarcinogenesis. Groups of rats were treated with aspartate salt of adenosine from the beginning of carcinogen administration for 12 or 18 weeks total, and another group received the compound from weeks 12 to 18. Fibrogenesis was estimated and the proportion of preneoplastic nodules and tumors was measured. The apoptotic and proliferation rates in liver tissues were evaluated, as well as the expression of cell signaling and cell cycle proteins participating in hepatocarcinogenesis. The adenosine derivative treatment reduced diethylnitrosamine-induced collagen expression and decreased the proportion of nodules positive for the tumor marker gamma-glutamyl transferase. This compound down-regulated the expression of thymidylate synthase and hepatocyte growth factor, and augmented the protein level of the cell cycle inhibitor p27; these effects could be part of its chemopreventive mechanism. These findings suggest a hepatoprotective role of aspartate salt of adenosine that could be used as a therapeutic compound in the prevention of liver tumorigenesis as described earlier for hepatic fibrosis. TUMOR BIOLOGY2017info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://repositorio.inmegen.gob.mx/record/14reponame:Repositorio del Instituto Nacional de Medicina Genómicainstname:Instituto Nacional de Medicina Genómicainstacron:INMIGENinfo:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc/4.0oai:repositorio.inmegen.gob.mx:142024-08-28T06:40:08Z
dc.title.none.fl_str_mv Cancer chemoprevention by an adenosine derivative in a model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in rats
title Cancer chemoprevention by an adenosine derivative in a model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in rats
spellingShingle Cancer chemoprevention by an adenosine derivative in a model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in rats
JULIO ISAEL PÉREZ CARREÓN
info:eu-repo/classification/cti/3
title_short Cancer chemoprevention by an adenosine derivative in a model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in rats
title_full Cancer chemoprevention by an adenosine derivative in a model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in rats
title_fullStr Cancer chemoprevention by an adenosine derivative in a model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in rats
title_full_unstemmed Cancer chemoprevention by an adenosine derivative in a model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in rats
title_sort Cancer chemoprevention by an adenosine derivative in a model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in rats
dc.creator.none.fl_str_mv JULIO ISAEL PÉREZ CARREÓN
author JULIO ISAEL PÉREZ CARREÓN
author_facet JULIO ISAEL PÉREZ CARREÓN
author_role author
dc.subject.none.fl_str_mv info:eu-repo/classification/cti/3
topic info:eu-repo/classification/cti/3
description Hepatocellular carcinoma is one of the most common cancers, and approximately 80% develop from cirrhotic livers. We have previously shown that the aspartate salt of adenosine prevents and reverses carbon tetrachloride-induced liver fibrosis in rats. Considering the hepatoprotective role of this adenosine derivative in fibrogenesis, we were interested in evaluating its effect in a hepatocarcinogenesis model induced by diethylnitrosamine in rats, where multinodular cancer is preceded by cirrhosis. Rats were injected with diethylnitrosamine for 12 weeks to induce cirrhosis and for 16 weeks to induce hepatocarcinogenesis. Groups of rats were treated with aspartate salt of adenosine from the beginning of carcinogen administration for 12 or 18 weeks total, and another group received the compound from weeks 12 to 18. Fibrogenesis was estimated and the proportion of preneoplastic nodules and tumors was measured. The apoptotic and proliferation rates in liver tissues were evaluated, as well as the expression of cell signaling and cell cycle proteins participating in hepatocarcinogenesis. The adenosine derivative treatment reduced diethylnitrosamine-induced collagen expression and decreased the proportion of nodules positive for the tumor marker gamma-glutamyl transferase. This compound down-regulated the expression of thymidylate synthase and hepatocyte growth factor, and augmented the protein level of the cell cycle inhibitor p27; these effects could be part of its chemopreventive mechanism. These findings suggest a hepatoprotective role of aspartate salt of adenosine that could be used as a therapeutic compound in the prevention of liver tumorigenesis as described earlier for hepatic fibrosis.
publishDate 2017
dc.date.none.fl_str_mv 2017
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://repositorio.inmegen.gob.mx/record/14
url http://repositorio.inmegen.gob.mx/record/14
dc.language.none.fl_str_mv
language_invalid_str_mv
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc/4.0
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by-nc/4.0
dc.format.none.fl_str_mv
dc.publisher.none.fl_str_mv TUMOR BIOLOGY
publisher.none.fl_str_mv TUMOR BIOLOGY
dc.source.none.fl_str_mv reponame:Repositorio del Instituto Nacional de Medicina Genómica
instname:Instituto Nacional de Medicina Genómica
instacron:INMIGEN
instname_str Instituto Nacional de Medicina Genómica
instacron_str INMIGEN
institution INMIGEN
reponame_str Repositorio del Instituto Nacional de Medicina Genómica
collection Repositorio del Instituto Nacional de Medicina Genómica
repository.name.fl_str_mv
repository.mail.fl_str_mv
_version_ 1858175206883852288
score 15,811543

Similares en LA Referencia