Microarray analysis of colon cancer cells treated with the pro-apoptotic drug lucanthone
Poster Number
7
Format
Poster Presentation
Faculty Mentor Name
Lisa Wrischnik
Additional Faculty Mentor Name
Uta Helhnann-Blumberg
Abstract/Artist Statement
Lucanthone, a drug previously used for the treatment of schistosome parasites, has been shown to help in the treatment of cancers. Based on preliminary studies, it has been shown that lucanthone induces cell death in various cancer cell lines, most notably cells lacking functional p53. p53 is a major tumor suppressor protein that either induces cells to stop dividing, a process known as cell cycle arrest, or to kill itself, a process known as apoptosis. In 50% of all tumors, p53 has been either mutated or knocked out. Therefore, a cancer treatment that can cause cell death in p53 deficient cells can be beneficial towards the treatment of many different tumors. It has been proposed that the reason for the induction of apoptosis is due to the activation of the cyclin dependent kinase inhibitor, p21. This is surprising since the major transcriptional activator for p21 is p53, yet since lucanthone induces apoptosis in p53 null cell lines, p21 must be activated in a p53-independent manner. Whereas p21 is typically known to cause cell cycle arrest, overexpression of the protein has been shown to induce apoptosis in a p53-independent manner. The purpose of this research project has been to elucidate the apoptosis pathway activated by leucanthone via the use ofrnicroarray experiments to check the expression levels of proteins in treated and untreated. cancer cells.
Location
Wendell Phillips Center, 1st floor hallways
Start Date
3-5-2008 1:00 PM
End Date
3-5-2008 3:00 PM
Microarray analysis of colon cancer cells treated with the pro-apoptotic drug lucanthone
Wendell Phillips Center, 1st floor hallways
Lucanthone, a drug previously used for the treatment of schistosome parasites, has been shown to help in the treatment of cancers. Based on preliminary studies, it has been shown that lucanthone induces cell death in various cancer cell lines, most notably cells lacking functional p53. p53 is a major tumor suppressor protein that either induces cells to stop dividing, a process known as cell cycle arrest, or to kill itself, a process known as apoptosis. In 50% of all tumors, p53 has been either mutated or knocked out. Therefore, a cancer treatment that can cause cell death in p53 deficient cells can be beneficial towards the treatment of many different tumors. It has been proposed that the reason for the induction of apoptosis is due to the activation of the cyclin dependent kinase inhibitor, p21. This is surprising since the major transcriptional activator for p21 is p53, yet since lucanthone induces apoptosis in p53 null cell lines, p21 must be activated in a p53-independent manner. Whereas p21 is typically known to cause cell cycle arrest, overexpression of the protein has been shown to induce apoptosis in a p53-independent manner. The purpose of this research project has been to elucidate the apoptosis pathway activated by leucanthone via the use ofrnicroarray experiments to check the expression levels of proteins in treated and untreated. cancer cells.