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Publication Date

Spring 5-10-2026

Keywords

Ewing Sarcoma, Pediatric Cancer, AKT, MTOR, Everolimus, Apoptosis, Proliferation, Migration, qRTPCR, Incucyte, Tissue Culture

Description

The purpose of this study is to use the gene AKT1, due to the interest in AKT1’s role in cancer cell proliferation, and the drug Everolimus, to determine if combined targeted therapy works as a more efficient therapeutic approach. Ewing Sarcoma has been connected to chromosomal translocations and is most common in pediatric patients. It is most often treated with chemotherapy and local treatments. It may be connected to the gene AKT1 due to how it regulates cell metabolism, growth, and proliferation. The gene mTOR is similarly connected to cell metabolism and proliferation, and is inhibited by the drug Everolimus. It has been hypothesized that AKT1 knockdown may increase Ewing Sarcoma’s sensitivity to Everolimus, potentially leading to an increase in apoptosis and a reduction in cell proliferation compared to drug use alone. If this is the case, then it would suggest that AKT1 normally protects cells from drug-induced stress. To test this, the AKT gene was knocked down using siRNA transfection and AKT and mTOR expression were measured and compared. Afterwards, 0.1 or 1.0 μM of Everolimus was added to some of the cells, and cell proliferation and apoptosis was measured. There was a significant difference between the groups, with the transfected cells showing the lowest expression of AKT and mTOR, and when combined with Everolimus, displayed the least amount of cell proliferation and survival.

Collection

Cell and Molecular Methods

Format

pdf

Size or Duration

14 Pages

City

San Antonio

Everolimus Treatment Combined With AKT1 Knockdown Increased Apoptosis and Decreased Cell Proliferation in Ewing Sarcoma Cells

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