Overview

My project explored the effects of melatonin on the planarian Schmidtea mediterranea and its applications to cancer. My research aimed to determine if melatonin would cause a change in these characteristics, such as cell proliferation and the expression of tumor suppressor genes. I found that melatonin decreased cell proliferation within these organisms, and I am currently in the process of determining how this hormone impacts tumor suppressor gene expression. Scroll to learn more about my project!

Abstract

Cancer, a disease characterized by the uncontrollable division of cells, is one of the leading causes of death worldwide. Current cancer treatments remain effective in the short term, but garner unwanted side effects and provide no guarantee of preventing relapse. These uncertainties have led researchers to look into alternative cancer treatments, such as 5-methoxy-N-acetyltryptamine, otherwise known as melatonin. This hormone has shown promising potential to be used as cancer treatment, as it is a naturally oncostatic agent with antiproliferative, antioxidative, and immunostimulatory mechanisms. The overall aim of this project is to demonstrate the anticancer effects of melatonin using a planarian model for cancer. With an abundant population of stem cells possessing a proliferative nature resembling that of cancer cells, the planarian Schmidtea mediterranea is an optimal model for studying this disease. Here, we focus on the effects of melatonin on cancer-like characteristics such as cell proliferation and tumor suppressor gene expression. When melatonin-dosed experimental groups were compared to the vehicular control, they displayed decreased cell proliferation and increased tumor suppressor gene expression, indicating melatonin’s ability to hinder cancer progression. Planarians possess molecular and biological features resembling that of mammals, making it reasonable to believe that these anticancer effects will present themselves in humans. The presence of these anticancer effects in an in-vivo model has the potential to advance oncological research, and promotes the use of melatonin as a novel treatment for cancer.

Figure 1

Figure 1: A depiction of average growth of planarian experimental groups dosed with various concentrations of melatonin and average growth of vehicular control group over a two week regeneration period. Average growth values (area of worms) from regeneration assays for 10⁻⁴ M, 10⁻⁵M, and 10⁻⁶ M melatonin concentrations are displayed. Error lines for standard error of the mean are included. Statistical significance has been indicated for each experimental group in comparison to the vehicular control.

Figure 2

Table 1: A depiction of p-values calculated from Mann-Whitney U Tests for experimental planarian groups dosed with melatonin in comparison to the vehicular control group. These p-values are indicated by the asterisks in Figure 1. All p-values were deemed to be highly statistically significant.

Figure 3

Figure 2: A depiction of average growth of planarian experimental groups dosed with melatonin and average growth of vehicular control group over the first seven days of regeneration and the final seven days for regeneration. Average growth values (area of worms) from regeneration assays for a 10⁻⁴ M melatonin concentrations are displayed. Error lines for standard error of the mean are included. Statistical significance has been indicated for each experimental group in comparison to the vehicular control.

Figure 4

Figure 3: A depiction of average growth of planarian experimental groups dosed with melatonin and average growth of vehicular control group over the first seven days of regeneration and the final seven days for regeneration. Average growth values (area of worms) from regeneration assays for a 10⁻⁵M melatonin concentrations are displayed. Error lines for standard error of the mean are included. Statistical significance has been indicated for each experimental group in comparison to the vehicular control.