Charles Okechukwu-Poster Presentation.
1
• T 3 reduced cell viability of MDA-MB-231 cells at the highest concentration but had no effect on the viability of the T47D cells • PPT significantly decreased cell viability of MDA-MB-231 but significantly enhanced cell viability of T47D • DPN significantly increased cell viability of T47D cells but had no effect on MDA-MB-231 cells. • Future direction would be to determine 1.) the modulation of receptor levels in breast cancer cells in absence or presence of T 3 and 2.) if T 3 promotes cell proliferation in the presence of diarylpropionitrile (DPN) and/or propyl- pyrozole-triol (PPT) . The involvement of estrogens in breast cancer development and growth has been established. However, we investigated the response of human breast cancer cells to thyroid hormone as well as the response of agonists of the estrogen receptor to breast cancer cells. More specifically, aim to determine the role of T 3 and/or estrogen agonists in the cell proliferation and viability of breast cancer cells. Using a tetrazolium-based colorimetric assay (MTT), we demonstrated that triiodothyronine (T 3 ) reduced the viability of MDA-MB-231 cells but enhanced the viability of T47D cells. In addition, both estrogen receptor agonists DPN and PPT enhanced the proliferation of T47D cells but had little to no effect on the viability of MDA-MB-231 cells. Based of these studies, we suggest that T 3 may play a role in the activation of the estrogen reporter in breast cancer cells. Future studies will be performed to determine the viability of breast cancer cells when treated both T 3 and agonists of the estrogen receptor. Contribution of thyroid hormone levels to estrogen receptor activation in breast cancer cells Charles Okechukwu,Dayami Lopez Ph.D., Carla Oldham Ph.D. Biomanufacturing Research Institute and Technology Enterprise (BRITE), North Carolina Central University Abstract In 2012, more than 300,000 new cases of breast cancer-related were diagnosed North American alone and it also affects more than 2,000 men each year [3]. Breast cancer (BC) occurs when malignant tumors develop in the breast. These cells can spread by breaking away from the original tumor and entering blood vessels or lymph vessels, which branch into tissues throughout the body. When cancer cells travel to other parts of the body and begin damaging other tissues and organs, the process is called metastasis. It is the third most widespread form of cancer amongst women in the world. The role of estrogen in breast cancer has been well established, with long-standing evidence that estrogen can both induce and promote breast cancer [1]. Evidence from epidemiologic studies has revealed a possible association between thyroid dysfunction and breast cancer. Material and Methods Conclusions Introduction (continued) Experimental Results 1.C.M.Klinge, S.C.Jernigan, K.A.Mattingly, et.al ,Estrogen response element-dependent regulation of transcriiptional activation of estrogen receptors alpha and beta by coactivators and corepressors,J.Mol.Endocrinal.33(2004)387-410. 2.Compton DR, Sheng S, Carlson KE, Rebacz NA, Lee IY, Katzenellenbogen BS, Katzenellenbogen JA 2004 Pyrazolo[1,5-a]pyrimidines: estrogen receptor ligands possessing estrogen receptor β antagonist activity. J References T47D Cell line MDA-MB-231 Cell line A B C D E F G H Figure 2. Effects of T 3 treatment on breast cancer cell viability. Culturing and T 3 treatment of the indicated breast cancer cell lines were done as described in Materials and Methods. Cell viability was detected using the MTT assay. Column and data points, mean percent viability relative to the control(n=4); bars, SE.A and B,Morphology representation of MDA-MB-231 cell and T47D cell line, C, effects of treatment with T 3 for 5d in T47D cell line, D, effects of treatment with T 3 for 5d in MDA-MB-231,E, Dose response of PPT on MDA-MB-231 cells,*,P<0.001,F,Dose response of DPN on MDA-MB-231 cells,G,Dose response of DPN on T47D cells,*,P<0.001,H,Dose Figure1. Subsets of Breast Cancer cells [3]. Figure 3.Experimental Design Risk factors include both genetic predisposition and environmental exposures such as diet, smoking, alcohol, etc. Breast Cancer deaths are declining because of early detection (mammogram) and treatment, including regularly scheduled, it has been successful in the early detection of adenomas, BC precursors. Our research focuses on the contribution of thyroid hormone level present in the activation of estrogen receptor in breast cancer. Specific Aims: • To determine the effects of T 3 on the viability of breast cancer cells; • To observe the effects of anti-cancer drugs on the viability of breast cancer in a hypothyroidism. Introduction
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Transcript of Charles Okechukwu-Poster Presentation.
• T3 reduced cell viability of MDA-MB-231 cells at the highest concentration but had no effect on the viability of the T47D cells
• PPT significantly decreased cell viability of MDA-MB-231 but significantly enhanced cell viability of T47D
• DPN significantly increased cell viability of T47D cells but had no effect on MDA-MB-231 cells.
• Future direction would be to determine 1.) the modulation of receptor levels in breast cancer cells in absence or presence of T3 and 2.) if T3 promotes cell proliferation in the presence of diarylpropionitrile (DPN) and/or propyl-pyrozole-triol (PPT) .
The involvement of estrogens in breast cancer development and growth has been established. However, we investigated the response of human breast cancer cells to thyroid hormone as well as the response of agonists of the estrogen receptor to breast cancer cells. More specifically, aim to determine the role of T3 and/or estrogen agonists in the cell proliferation and viability of breast cancer cells. Using a tetrazolium-based colorimetric assay (MTT), we demonstrated that triiodothyronine (T3) reduced the viability of MDA-MB-231 cells but enhanced the viability of T47D cells. In addition, both estrogen receptor agonists DPN and PPT enhanced the proliferation of T47D cells but had little to no effect on the viability of MDA-MB-231 cells. Based of these studies, we suggest that T3 may play a role in the activation of the estrogen reporter in breast cancer cells. Future studies will be performed to determine the viability of breast cancer cells when treated both T3 and agonists of the estrogen receptor.
Contribution of thyroid hormone levels to estrogen receptor activation in breast cancer cells
Charles Okechukwu,Dayami Lopez Ph.D., Carla Oldham Ph.D.
Biomanufacturing Research Institute and Technology Enterprise (BRITE), North Carolina Central UniversityAbstract
In 2012, more than 300,000 new cases of breast cancer-related were diagnosed North American alone and it also affects more than 2,000 men each year [3]. Breast cancer (BC) occurs when malignant tumors develop in the breast. These cells can spread by breaking away from the original tumor and entering blood vessels or lymph vessels, which branch into tissues throughout the body. When cancer cells travel to other parts of the body and begin damaging other tissues and organs, the process is called metastasis. It is the third most widespread form of cancer amongst women in the world.The role of estrogen in breast cancer has been well established, with long-standing evidence that estrogen can both induce and promote breast cancer [1]. Evidence from epidemiologic studies has revealed a possible association between thyroid dysfunction and breast cancer. Hyperthyroidism was found in postmenopausal, but not in premenopausal, breast cancer patients [2]. However, neither the epidemiologic or in vitro data provide a definitive picture of significance of T3 in the etiology of breast cancer [2].
Material and Methods
Conclusions
Introduction (continued)
Experimental Results
1.C.M.Klinge, S.C.Jernigan, K.A.Mattingly, et.al ,Estrogen response element-dependent regulation of transcriiptional activation of estrogen receptors alpha and beta by coactivators and corepressors,J.Mol.Endocrinal.33(2004)387-410.
2.Compton DR, Sheng S, Carlson KE, Rebacz NA, Lee IY, Katzenellenbogen BS, Katzenellenbogen JA 2004 Pyrazolo[1,5-a]pyrimidines: estrogen receptor ligands possessing estrogen receptor β antagonist activity. J Med Chem 47:5872–5893.3. American Cancer Society:Cancer facts & figures 2010.
References
T47D Cell line MDA-MB-231 Cell line
A B C D
E F G H
Figure 2. Effects of T3 treatment on breast cancer cell viability. Culturing and T3 treatment of the indicated breast cancer cell lines were done as described in Materials and Methods. Cell viability was detected using the MTT assay. Column and data points, mean percent viability relative to the control(n=4); bars, SE.A and B,Morphology representation of MDA-MB-231 cell and T47D cell line, C, effects of treatment with T3 for 5d in T47D cell line, D, effects of treatment with T3 for 5d in MDA-MB-231,E, Dose response of PPT on MDA-MB-231 cells,*,P<0.001,F,Dose response of DPN on MDA-MB-231 cells,G,Dose response of DPN on T47D cells,*,P<0.001,H,Dose response for T3 in T47D cells,*,P<0.001.Note : All treatment was carried out for 5d.
Figure1. Subsets of BreastCancer cells [3].
Figure 3.Experimental Design
Risk factors include both genetic predisposition and environmental exposures such as diet, smoking, alcohol, etc. Breast Cancer deaths are declining because of early detection (mammogram) and treatment, including regularly scheduled, it has been successful in the early detection of adenomas, BC precursors. Our research focuses on the contribution of thyroid hormone level present in the activation of estrogen receptor in breast cancer.
Specific Aims:• To determine the effects of T3 on the viability of breast cancer cells;• To observe the effects of anti-cancer drugs on the viability of breast cancer in a hypothyroidism.
Introduction
