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dc.contributor.authorShah, Anil Ajiten_US
dc.date.accessioned2016-03-02T16:44:32Z
dc.date.available2016-03-02T16:44:32Z
dc.date.issued2014
dc.identifier.urihttps://hdl.handle.net/2144/14684
dc.description.abstractBreast cancer is the second most common type of cancer among women. The serine-threonine protein kinase CK2 is overexpressed in many cancers, including lung, prostate, hematologic cancers, and breast (Pinna, 2013). Here, we examined the potential of CK2 inhibition alone and in combination with chemotherapy to treat breast cancer. We performed cell viability assays on five breast cancer cell lines treated with CK2 chemical inhibitors or small interfering RNAs, and chemotherapeutic drugs, to test if a synergistic effect could be attained. We also tested if CK2 inhibition would change the stem-like phenotype, epithelial-to-mesenchymal (EMT) marker expression, and CK2 subunit gene expression in the HS578T cell line. We concluded that in the five cell lines utilized, CK2 inhibition had no synergistic effect with chemotherapeutic drugs. CK2 inhibition had no effect on the stem-like phenotype of HS578T cells. However, CK2 inhibition did show a pattern of inhibition of EMT marker expression. Finally, we found that CK2 inhibition appears to activate a compensatory feedback loop for the transcription of the alpha subunit. This may explain the lack of synergy, and bears further investigation in future studies.en_US
dc.language.isoen_US
dc.subjectMedicineen_US
dc.titleExploratory role of protein kinase CK2 synergy in treatment of breast canceren_US
dc.typeThesis/Dissertationen_US
dc.date.updated2016-01-22T18:57:31Z
etd.degree.nameMaster of Scienceen_US
etd.degree.levelmastersen_US
etd.degree.disciplineMedical Sciencesen_US
etd.degree.grantorBoston Universityen_US


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