Document Type

Article

Publication Date

5-25-2017

Scholarship Domain(s)

Scholarship of Discovery

Abstract

One of the most commonly found mutations in cancers is a mutation in p53. A mutation in p53 does not allow the cell to correct DNA damage or mutations properly, leading to uncontrolled growth and a tumor. α-Mangostin is a p53 activator found in a fruit from Southeast Asia, and when applied to cells, it will arrest them in the S phase. Paclitaxel is a chemotherapy that kills cells as they enter mitosis. Arrested cells will not enter mitosis and therefore will not be killed by paclitaxel. Because of mutated dysfunctional p53, cancer cells are not susceptible to arrest by the p53 activator and therefore can still be killed by paclitaxel. This technique of selectively killing cancer cells while protecting the healthy cells is called chemoprotection. It allows doctors to use higher dosages of chemotherapy without the side effects because of damage to the healthy cells. The purpose of this study is to determine if α-mangostin, a potential chemoprotectant, can be used to protect BHK cells from the cytotoxic effects of paclitaxel. Because α-mangostin is an anti-proliferative, treating the cells with α-mangostin decreases total cell number in a dose dependent manner. Interestingly, I found that pretreating cells with increasing concentrations of α-mangostin before treating them with paclitaxel increased the total cell number per well when compared to cells treated with paclitaxel alone until the toxic concentration of α-mangostin. This finding indicates that α-mangostin may be a good candidate for a chemoprotectant to be used when treating cancer patients.

Comments

Faculty Advisor, Greg Long. Honors Cohort 7. Graduation date 2017.

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