Archer’s annual STEM Symposium is an opportunity for Los Angeles high school students who have completed independent or small group projects in STEM to present their findings. Students are invited to present their research in the fields of molecular biology, chemistry, physics, and engineering.
The Archer RISE Award honors exceptional young women for their innovative scientific research or engineering design projects that further existing knowledge or develop solutions to pressing scientific challenges. Finalists for the RISE Award are noted in throughout the online program and will be awarded at lunch on May 21.
Methyl Jasmonate (MeJA), a plant stress hormone, has been shown to selectively target cancer cells and induce apoptosis by dissociating hexokinase, a key enzyme in the glycolytic pathway that is overexpressed in cancer cells, from the outer mitochondrial membrane. Because MeJA uses the glycolytic pathway to induce apoptosis, specifically targeting hexokinase, it functions well as a selective cytotoxic agent and sensitizes other chemotherapeutic agents to have increased efficacy in cancer cytotoxicity. Perillyl Alcohol (POH), a plant-derived hormone, has been used in combination therapies for cancer treatment and has been found to have similar sensitizing cytotoxic effects to MeJA. Although it has successfully induced apoptosis in a variety of cell lines, the mechanisms by which POH acts are unknown . In this study we aimed to contribute to the characterization of POH[?]s apoptotic mechanisms through a comparative study of combination treatments between MeJA and POH with common chemotherapeutic agents (cisplatin and etoposide). Cytotoxicity levels were tested in SKBR3 breast cancer cell lines and assayed using the Sulforhodamine B dye and microplate readers. In addition to the SKBR3 cell lines we tested two mutants of the same cell lines that express the molecules tDrrp and T75A. tDrrp is the truncated form of a protein that allows breast cancer to become resistant to herceptin treatment; T75A is tDrrp’s mutant that is supposed to render it inactive. Our research progressed to a data collection and analysis of POH and MJ combination effects on tDrrp expressing cancer cells, and normal cancer cells.