Title : β-Thujaplicin modulates estrogen receptor signaling and inhibits proliferation of human breast cancer cells.

Pub. Date : 2015

PMID : 25666914






5 Functional Relationships(s)
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1 In this study, we found that beta-thujaplicin significantly suppressed the proliferation through arresting the cell cycle transition from G1 to S phase as well as inhibited the expression of cell cycle-related proteins, cyclin D1, and cyclin-dependent kinase 4 (CDK4) in MCF-7 and T47D luminal subtype breast cancer cells. beta-thujaplicin cyclin D1 Homo sapiens
2 In this study, we found that beta-thujaplicin significantly suppressed the proliferation through arresting the cell cycle transition from G1 to S phase as well as inhibited the expression of cell cycle-related proteins, cyclin D1, and cyclin-dependent kinase 4 (CDK4) in MCF-7 and T47D luminal subtype breast cancer cells. beta-thujaplicin cyclin dependent kinase 4 Homo sapiens
3 In this study, we found that beta-thujaplicin significantly suppressed the proliferation through arresting the cell cycle transition from G1 to S phase as well as inhibited the expression of cell cycle-related proteins, cyclin D1, and cyclin-dependent kinase 4 (CDK4) in MCF-7 and T47D luminal subtype breast cancer cells. beta-thujaplicin cyclin dependent kinase 4 Homo sapiens
4 In addition, estrogen receptor alpha (ER-alpha) was down-regulated by beta-thujaplicin via enhanced proteolysis by ubiquitination, which led to cell growth inhibition. beta-thujaplicin estrogen receptor 1 Homo sapiens
5 In addition, estrogen receptor alpha (ER-alpha) was down-regulated by beta-thujaplicin via enhanced proteolysis by ubiquitination, which led to cell growth inhibition. beta-thujaplicin estrogen receptor 1 Homo sapiens