The effects of iPLA2β (Ca2+-independent Phospholipase A2β) and MMP-9 (Matrix Metalloproteinase-9) have been a recent focus of research in the progression of cancer cell proliferation and migration. However, their roles are not entirely known, especially concerning nicotine-induced breast cancer cell advancement. The purpose of this study was to determine the involvement of iPLA2β in nicotine-induced breast cancer cell proliferation. BEL (bromoenol lactone), a suicide inhibitor of iPLA2β, was hypothesized to attenuate nicotine-induced breast cancer cell proliferation and tumor growth. Following the BEL treatment, the in-vitro results exhibited a significant decrease in 4T1 cell proliferation for both basal and nicotine-induced, as shown by MTT proliferation assays. Scratch and transwell assays revealed migration was also significantly attenuated. In addition, the expression of MMP-9 was discovered to have expressed in an iPLA2β-dependent manner, which further supports the idea that iPLA2β plays a significant role, concerning the mediation of basal and nicotine-induced cancer cell progression. Our in-vivo results also supported this conclusion. In mice, basal and nicotine-induced tumor growth was significantly decreased, in comparison with the control group. The presence of nicotine-induced tumors in lung tissue was reduced significantly. In-vitro and in-vivo results suggest that iPLA2β plays a critical role in the regulation of breast cancer cell proliferation and migration and is found upstream of MMP-9. In addition, nicotine-induced breast cancer is promoted through iPLA2β expression. Because BEL was found to reduce the effects of this, it may be a possible chemotherapeutic drug to clinically develop.

Semester/Year of Award

Fall 2016


Lindsay E. Calderon

Department/Professional Affiliation

Biological Sciences

Access Options

Open Access Thesis

Degree Name

Honors Scholars


Biological Sciences