Abstract

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

Mentor

Lindsay E. Calderon

Mentor Professional Affiliation

Biological Sciences

Access Options

Open Access Thesis

Document Type

Bachelor Thesis

Degree Name

Honors Scholars

Degree Level

Bachelor's

Department

Biological Sciences

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