Recently in the world, there has been a rapid increase in the prevalence of and mortality from obesity, diabetes mellitus, and colorectal cancer (CRC). Colorectal cancer related deaths have become the second highest category of cancer death in both the U.S. and the world, including roughly 2 million global diagnoses every year and 700,000 CRC related deaths. Estrogen has been shown in past studies to prevent CRC incidence and to slow CRC progression in women. Studies have also shown that pre-menopausal women are less likely to develop CRC than men. Hormone replacement therapies in post-menopausal women have suggested that the main female sex hormone, estradiol (E2), is largely effective in reducing the growth of CRC. Additionally, high plasma glucose levels associated with type-2 diabetes and higher leptin levels associated with obesity could be responsible for the formation or metastasis and migration of CRC cells. In our experiment, Human noncancerous CCD cells (normal control) and CRC cells (Caco-2, Lovo, and HCT116) were grown in DMEM media, with nutrients and antibiotics at three different glucose concentrations, no (0 g/L), low (1 g/L) and high (4.5 g/L). BrdU assay was used to assess proliferation by utilizing a tagged thymidine-analog in dividing cells. Caspase-3/7 substrates were used that demonstrate activity proportional to caspase activity as an indicator of apoptosis. Our results have indicated that high glucose levels in certain CRC cells promote cell proliferation indicated by BrdU incorporation; and E2 reverses leptin-induced CRC cell proliferation. Therefore, obesity hormone leptin may contribute to CRC progression, while estrogen may prevent CRC progression induced by leptin. This study may contribute to development of new prevention strategies and therapies for colorectal cancer.
Author(s): Charles Schaeffer, Biology and Music Performance Major
Advisor(s): Haifei Shi, Department of Biology
Flora Xi, Department of Biology
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