Shaun Karakkattu

Shaun Karakkattu, Basis High School, Mesa, AZ

Inhibiting the Proliferation of Patient-Derived Glioblastoma Multiforme (GBM) cells by activating Estrogen Receptor beta using estradiol and IGF-1

 

Glioblastoma multiforme (GBM) is the most aggressive and common type of primary brain tumor. Patients with GBM have a median survival rate between 12-14 months. There are sex-based differences that exist in the occurance of GBM with men having a 60% higher chance of developing a tumor indicating that differences in the function of Estrogen Receptor Beta (ERβ), a known tumor suppressor, may influence tumor progression in GBM. Considering ERβ function, it was hypothesized that 17β-estradiol and IGF-1, estrogen receptor agonists, may promote ERβ function and inhibit the proliferation of GBM cells in vitro. 17β-estradiol and IGF-1 were applied to a patient-derived GBM cell line and MDA-MB-453, breast cancer cell line, in-vitro. The concentrations tested ranged from 2 to 20 µg/mL of 17β-estradiol and IGF-1. After 48 hrs of exposure, GBM cell proliferation was analyzed through a trypan blue exclusion assay. The results revealed that cell proliferation was inhibited by the estrogen receptor agonists in the patient-derived GBM cells and promoted in the MDA-MB-453 cell line which served as a positive control. In conclusion, this study presents evidence that ERβ function may indeed inhibit GBM proliferation. This study presents a potential approach to the treatment of GBM. As this study continues, more steroid hormone receptors will be tested like the Androgen Receptor which may also cause the inhibition of cell proliferation in GBM.

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