The Effects Of Emodin On Macrophage-Cancer Cell Interaction

Wenxin Fan

School Name

Spring Valley High School

Grade Level

11th Grade

Presentation Topic

Cell and Molecular Biology

Presentation Type

Mentored

Mentor

Mentor: Dr. Angela Murphy; University of South Carolina School of Medicine

Oral Presentation Award

1st Place

Written Paper Award

2nd Place

Abstract

Cancer results from mutations that cause alterations in cell function, growth and division. Malignant tumors formed of cancerous cells can lead to disruptions in systemic functions. A growing method of treatment for cancer is immunotherapy. The purpose of this study was to explore the potential of emodin as an anti-tumor treatment through modulating immune cell-cancer cell interaction. The specific mechanisms by which emodin affects cancer cell interactions were examined, including its impact on the expression of mannose receptor (MR), a protein found on the surface of macrophages. It was hypothesized that if emodin is used to treat macrophages, a lower concentration of MR would be produced in comparison to macrophages that were not treated with emodin. It was also hypothesized that if emodin-treated macrophages were applied to cancer cells, a lower number of adherences would occur. A positive correlation of higher MR concentration to higher adherence may indicate a possible mechanism behind cancer cell and macrophage interaction. Emodin concentrations of 0 µM, 10 µM, and 30 µM were used to treat macrophages and real-time PCR was conduced to measure the relative expression levels of MR. An ANOVA determined that the groups were significantly different; F(3,8)=80.8, p<0.05, and that emodin at the highest concentration significantly reduced the expression of MR on macrophages. Macrophages treated with the various concentrations of emodin were applied to cancer cells and allowed them to interact and adhere to each other. Non-adherent macrophages were subsequently washed away and the adherent macrophages were examined and counted under a microscope. An ANOVA determined that the counts among the groups were significantly different; F(3,156)=8.04, p<0.05, and in particular, the highest emodin concentration treatment suppressed the adhesion between macrophages and cancer cells. In conclusion, the hypotheses were supported and emodin may be used as a therapy for cancer.

Location

Owens 202

Start Date

4-16-2016 10:00 AM

COinS
 
Apr 16th, 10:00 AM

The Effects Of Emodin On Macrophage-Cancer Cell Interaction

Owens 202

Cancer results from mutations that cause alterations in cell function, growth and division. Malignant tumors formed of cancerous cells can lead to disruptions in systemic functions. A growing method of treatment for cancer is immunotherapy. The purpose of this study was to explore the potential of emodin as an anti-tumor treatment through modulating immune cell-cancer cell interaction. The specific mechanisms by which emodin affects cancer cell interactions were examined, including its impact on the expression of mannose receptor (MR), a protein found on the surface of macrophages. It was hypothesized that if emodin is used to treat macrophages, a lower concentration of MR would be produced in comparison to macrophages that were not treated with emodin. It was also hypothesized that if emodin-treated macrophages were applied to cancer cells, a lower number of adherences would occur. A positive correlation of higher MR concentration to higher adherence may indicate a possible mechanism behind cancer cell and macrophage interaction. Emodin concentrations of 0 µM, 10 µM, and 30 µM were used to treat macrophages and real-time PCR was conduced to measure the relative expression levels of MR. An ANOVA determined that the groups were significantly different; F(3,8)=80.8, p<0.05, and that emodin at the highest concentration significantly reduced the expression of MR on macrophages. Macrophages treated with the various concentrations of emodin were applied to cancer cells and allowed them to interact and adhere to each other. Non-adherent macrophages were subsequently washed away and the adherent macrophages were examined and counted under a microscope. An ANOVA determined that the counts among the groups were significantly different; F(3,156)=8.04, p<0.05, and in particular, the highest emodin concentration treatment suppressed the adhesion between macrophages and cancer cells. In conclusion, the hypotheses were supported and emodin may be used as a therapy for cancer.