Hypothyroidism reduces mammary tumor progression via [Beta]-catenin-activated intrinsic apoptotic pathway in rats
Experimental hypothyroidism retards mammary carcinogenesis promoting apoptosis of tumor cells. [beta]-catenin plays a critical role in cell adhesion and intracellular signaling pathways conditioning the prognosis of breast cancer. However, the mechanistic connections associated with the expression o...
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| Veröffentlicht in: | Histochemistry and cell biology 2017-06, Vol.147 (6), p.759 |
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| creator | López Fontana, C M Zyla, L E Santiano, F E Sasso, C V Cuello-carrión, F D Pistone Creydt, V Fanelli, M A Carón, R W |
| description | Experimental hypothyroidism retards mammary carcinogenesis promoting apoptosis of tumor cells. [beta]-catenin plays a critical role in cell adhesion and intracellular signaling pathways conditioning the prognosis of breast cancer. However, the mechanistic connections associated with the expression of [beta]-catenin in thyroid status and breast cancer are not known. Therefore, we studied the relationship between the expression and localization of [beta]-catenin and apoptosis in mammary tumors induced by 7,12-dimethylbenz(a)anthracene (DMBA) in hypothyroid (Hypot) and euthyroid (EUT) rats. Female Sprague Dawley rats were treated with a dose of DMBA (15 mg/rat) at 55 days of age and were then divided into two groups: HypoT (0.01% 6-N-propyl-2-thiouracil in drinking water, n=54) and EUT (untreated control, n=43). Latency, incidence and progression of tumors were determined. At sacrifice, tumors were obtained for immunohistological studies and Western Blot. The latency was longer (p |
| doi_str_mv | 10.1007/s00418-017-1544-x |
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[beta]-catenin plays a critical role in cell adhesion and intracellular signaling pathways conditioning the prognosis of breast cancer. However, the mechanistic connections associated with the expression of [beta]-catenin in thyroid status and breast cancer are not known. Therefore, we studied the relationship between the expression and localization of [beta]-catenin and apoptosis in mammary tumors induced by 7,12-dimethylbenz(a)anthracene (DMBA) in hypothyroid (Hypot) and euthyroid (EUT) rats. Female Sprague Dawley rats were treated with a dose of DMBA (15 mg/rat) at 55 days of age and were then divided into two groups: HypoT (0.01% 6-N-propyl-2-thiouracil in drinking water, n=54) and EUT (untreated control, n=43). Latency, incidence and progression of tumors were determined. At sacrifice, tumors were obtained for immunohistological studies and Western Blot. The latency was longer (p<0.05), the incidence was lower (p<0.0001) and tumor growth was slower (p<0.01) in HypoT rats compared to EUT. The expression of Bax, cleaved caspase-9 and caspase-3 was significantly higher in tumors of HypoT than in EUT (p<0.05) indicating the activation of the intrinsic pathway. In this group, [beta]-catenin was expressed in the plasma membrane and with less intensity, while its expression was nuclear and with greater intensity in the EUT (p<0.05). Moreover, the expression of survivin was reduced in tumors of HypoT rats (p<0.05). In conclusion, decreased expression of [beta]-catenin and its normal location in membrane of mammary tumors are associated with augmented apoptosis via activation of the intrinsic pathway in HypoT rats.]]></description><identifier>ISSN: 0948-6143</identifier><identifier>EISSN: 1432-119X</identifier><identifier>DOI: 10.1007/s00418-017-1544-x</identifier><language>eng</language><publisher>New York: Springer Nature B.V</publisher><subject>9,10-Dimethyl-1,2-benzanthracene ; Anthracene ; Apoptosis ; Breast cancer ; Carcinogenesis ; Caspase ; Caspase-3 ; Caspase-9 ; Cell adhesion ; Cell adhesion & migration ; Drinking water ; Hypothyroidism ; Intracellular signalling ; Latency ; Localization ; Mammary gland ; Rodents ; Survivin ; Thyroid cancer ; Tumor cells ; Tumors ; β-Catenin</subject><ispartof>Histochemistry and cell biology, 2017-06, Vol.147 (6), p.759</ispartof><rights>Histochemistry and Cell Biology is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>López Fontana, C M</creatorcontrib><creatorcontrib>Zyla, L E</creatorcontrib><creatorcontrib>Santiano, F E</creatorcontrib><creatorcontrib>Sasso, C V</creatorcontrib><creatorcontrib>Cuello-carrión, F D</creatorcontrib><creatorcontrib>Pistone Creydt, V</creatorcontrib><creatorcontrib>Fanelli, M A</creatorcontrib><creatorcontrib>Carón, R W</creatorcontrib><title>Hypothyroidism reduces mammary tumor progression via [Beta]-catenin-activated intrinsic apoptotic pathway in rats</title><title>Histochemistry and cell biology</title><description><![CDATA[Experimental hypothyroidism retards mammary carcinogenesis promoting apoptosis of tumor cells. [beta]-catenin plays a critical role in cell adhesion and intracellular signaling pathways conditioning the prognosis of breast cancer. However, the mechanistic connections associated with the expression of [beta]-catenin in thyroid status and breast cancer are not known. Therefore, we studied the relationship between the expression and localization of [beta]-catenin and apoptosis in mammary tumors induced by 7,12-dimethylbenz(a)anthracene (DMBA) in hypothyroid (Hypot) and euthyroid (EUT) rats. Female Sprague Dawley rats were treated with a dose of DMBA (15 mg/rat) at 55 days of age and were then divided into two groups: HypoT (0.01% 6-N-propyl-2-thiouracil in drinking water, n=54) and EUT (untreated control, n=43). Latency, incidence and progression of tumors were determined. At sacrifice, tumors were obtained for immunohistological studies and Western Blot. The latency was longer (p<0.05), the incidence was lower (p<0.0001) and tumor growth was slower (p<0.01) in HypoT rats compared to EUT. The expression of Bax, cleaved caspase-9 and caspase-3 was significantly higher in tumors of HypoT than in EUT (p<0.05) indicating the activation of the intrinsic pathway. In this group, [beta]-catenin was expressed in the plasma membrane and with less intensity, while its expression was nuclear and with greater intensity in the EUT (p<0.05). Moreover, the expression of survivin was reduced in tumors of HypoT rats (p<0.05). In conclusion, decreased expression of [beta]-catenin and its normal location in membrane of mammary tumors are associated with augmented apoptosis via activation of the intrinsic pathway in HypoT rats.]]></description><subject>9,10-Dimethyl-1,2-benzanthracene</subject><subject>Anthracene</subject><subject>Apoptosis</subject><subject>Breast cancer</subject><subject>Carcinogenesis</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Caspase-9</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Drinking water</subject><subject>Hypothyroidism</subject><subject>Intracellular signalling</subject><subject>Latency</subject><subject>Localization</subject><subject>Mammary gland</subject><subject>Rodents</subject><subject>Survivin</subject><subject>Thyroid cancer</subject><subject>Tumor cells</subject><subject>Tumors</subject><subject>β-Catenin</subject><issn>0948-6143</issn><issn>1432-119X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNjc1KxDAUhYMoWH8ewF3AdTS3k2mbraLMA7gQRIZLG50M5mdyb0f79mbhA7g6H-c7cIS4AX0HWvf3pLWBQWnoFayNUT8nogGzahWAfT0VjbZmUF1tzsUF0V5rWNu2bcRhs-TEu6UkP3kKsrhpHh3JgCFgWSTPIRWZS_osjsinKI8e5duDY3xXI7KLPioc2R8rT9JHLj6SHyXmlDlxpYy8-8alOlmQ6UqcfeAXueu_vBS3z08vjxtVTw6zI97u01xiVVsYrO2s6aBf_W_1Cx0rU_w</recordid><startdate>20170601</startdate><enddate>20170601</enddate><creator>López Fontana, C M</creator><creator>Zyla, L E</creator><creator>Santiano, F E</creator><creator>Sasso, C V</creator><creator>Cuello-carrión, F D</creator><creator>Pistone Creydt, V</creator><creator>Fanelli, M A</creator><creator>Carón, R W</creator><general>Springer Nature B.V</general><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20170601</creationdate><title>Hypothyroidism reduces mammary tumor progression via [Beta]-catenin-activated intrinsic apoptotic pathway in rats</title><author>López Fontana, C M ; Zyla, L E ; Santiano, F E ; Sasso, C V ; Cuello-carrión, F D ; Pistone Creydt, V ; Fanelli, M A ; Carón, R W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_journals_18996946173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>9,10-Dimethyl-1,2-benzanthracene</topic><topic>Anthracene</topic><topic>Apoptosis</topic><topic>Breast cancer</topic><topic>Carcinogenesis</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Caspase-9</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Drinking water</topic><topic>Hypothyroidism</topic><topic>Intracellular signalling</topic><topic>Latency</topic><topic>Localization</topic><topic>Mammary gland</topic><topic>Rodents</topic><topic>Survivin</topic><topic>Thyroid cancer</topic><topic>Tumor cells</topic><topic>Tumors</topic><topic>β-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>López Fontana, C M</creatorcontrib><creatorcontrib>Zyla, L E</creatorcontrib><creatorcontrib>Santiano, F E</creatorcontrib><creatorcontrib>Sasso, C V</creatorcontrib><creatorcontrib>Cuello-carrión, F D</creatorcontrib><creatorcontrib>Pistone Creydt, V</creatorcontrib><creatorcontrib>Fanelli, M A</creatorcontrib><creatorcontrib>Carón, R W</creatorcontrib><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Histochemistry and cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>López Fontana, C M</au><au>Zyla, L E</au><au>Santiano, F E</au><au>Sasso, C V</au><au>Cuello-carrión, F D</au><au>Pistone Creydt, V</au><au>Fanelli, M A</au><au>Carón, R W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypothyroidism reduces mammary tumor progression via [Beta]-catenin-activated intrinsic apoptotic pathway in rats</atitle><jtitle>Histochemistry and cell biology</jtitle><date>2017-06-01</date><risdate>2017</risdate><volume>147</volume><issue>6</issue><spage>759</spage><pages>759-</pages><issn>0948-6143</issn><eissn>1432-119X</eissn><abstract><![CDATA[Experimental hypothyroidism retards mammary carcinogenesis promoting apoptosis of tumor cells. [beta]-catenin plays a critical role in cell adhesion and intracellular signaling pathways conditioning the prognosis of breast cancer. However, the mechanistic connections associated with the expression of [beta]-catenin in thyroid status and breast cancer are not known. Therefore, we studied the relationship between the expression and localization of [beta]-catenin and apoptosis in mammary tumors induced by 7,12-dimethylbenz(a)anthracene (DMBA) in hypothyroid (Hypot) and euthyroid (EUT) rats. Female Sprague Dawley rats were treated with a dose of DMBA (15 mg/rat) at 55 days of age and were then divided into two groups: HypoT (0.01% 6-N-propyl-2-thiouracil in drinking water, n=54) and EUT (untreated control, n=43). Latency, incidence and progression of tumors were determined. At sacrifice, tumors were obtained for immunohistological studies and Western Blot. The latency was longer (p<0.05), the incidence was lower (p<0.0001) and tumor growth was slower (p<0.01) in HypoT rats compared to EUT. The expression of Bax, cleaved caspase-9 and caspase-3 was significantly higher in tumors of HypoT than in EUT (p<0.05) indicating the activation of the intrinsic pathway. In this group, [beta]-catenin was expressed in the plasma membrane and with less intensity, while its expression was nuclear and with greater intensity in the EUT (p<0.05). Moreover, the expression of survivin was reduced in tumors of HypoT rats (p<0.05). In conclusion, decreased expression of [beta]-catenin and its normal location in membrane of mammary tumors are associated with augmented apoptosis via activation of the intrinsic pathway in HypoT rats.]]></abstract><cop>New York</cop><pub>Springer Nature B.V</pub><doi>10.1007/s00418-017-1544-x</doi></addata></record> |
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| subjects | 9,10-Dimethyl-1,2-benzanthracene Anthracene Apoptosis Breast cancer Carcinogenesis Caspase Caspase-3 Caspase-9 Cell adhesion Cell adhesion & migration Drinking water Hypothyroidism Intracellular signalling Latency Localization Mammary gland Rodents Survivin Thyroid cancer Tumor cells Tumors β-Catenin |
| title | Hypothyroidism reduces mammary tumor progression via [Beta]-catenin-activated intrinsic apoptotic pathway in rats |
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