| dc.description.abstract | Breast cancer is the most common cancer in women and is predominantly estrogen dependent [1]. About 1 in 8 women in the United States (12%) will develop invasive breast cancer over the course of her lifetime. Failure in the current treatment of breast cancer has led to an increased desire to find the specific mechanism of how cancer cell proliferation is inhibited. G protein-coupled estrogen receptor (GPER) is very controversial when concerning breast cancer cell proliferation. Some studies report evidence that GPER is strongly associated with increased cancer proliferation, migration, invasion, differentiation and metastasis [2]. Other studies have found that GPER inhibits proliferation of MCF-7 breast cancer cells [3]. The objective of this study was to clarify whether GPER works to promote or inhibit MCF-7 breast cancer cell proliferation. I found that G-1 (GPER agonist) acted on GPER to inhibit MCF-7 cell proliferation. Manual cell counting was used to find the doubling time of the MCF-7 cells. To determine the effect of G-1 on the cells proliferation I used a cell proliferation assay kit. Through this method it was found that G-1 inhibits proliferation in a concentration dependent manner. Western blot was used to detect the target proteins such as GPER, ER, ER, p53 and p38. I tested antibody on these cells through Western blot and discovered that the correct antibodies were used and p38 and p53 proteins were present in the MCF-7 cells. Immunocytochemistry was also used to test specific antibodies. Proliferating Cell Nuclear Antigen (PCNA) antibody and -actin antibody were tested using this method. These results demonstrated that GPER activation inhibits MCF-7 cell proliferation. | en |
