Presentation Title

The Effects of P53 Wild Type and two of its mutants of MCF-7 cells

Faculty Mentor

Luiza Nogaj

Start Date

17-11-2018 8:30 AM

End Date

17-11-2018 10:30 AM

Location

CREVELING 89

Session

POSTER 1

Type of Presentation

Poster

Subject Area

biological_agricultural_sciences

Abstract

P53 is a tumor suppressor protein responsible for regulating cell proliferation. When activated by DNA damage or oncogenic activity, P53 induces apoptosis, cell cycle arrest, or senescence. Various types of cancers worldwide are associated with P53 mutations especially those located in the DNA binding domain. Of these mutations, R248Q and R248W are most commonly seen in cancer patients. Mutations of P53 affect its structure and function, resulting in P53 gaining oncogenic functions. The focus of this research is to identify the effects WT and the R248Q and R248W mutants on mammalian cells. Molecular cloning techniques, such as PCR, were used to clone full length P53 and the mutations 248Q and 248W into pcDNA3.1. Cellular assays, such as MTT and cytotoxicity, were utilized in determining the effects of WT P53, R248Q, and R248W on MCF-7 cells. Preliminary results show that full length WT P53 decreases cell viability, while 248Q and 248W increase the MCF-7 viability. Further analysis is necessary to determine the effects of P53 mutants on DNA binding and cell proliferation.

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Nov 17th, 8:30 AM Nov 17th, 10:30 AM

The Effects of P53 Wild Type and two of its mutants of MCF-7 cells

CREVELING 89

P53 is a tumor suppressor protein responsible for regulating cell proliferation. When activated by DNA damage or oncogenic activity, P53 induces apoptosis, cell cycle arrest, or senescence. Various types of cancers worldwide are associated with P53 mutations especially those located in the DNA binding domain. Of these mutations, R248Q and R248W are most commonly seen in cancer patients. Mutations of P53 affect its structure and function, resulting in P53 gaining oncogenic functions. The focus of this research is to identify the effects WT and the R248Q and R248W mutants on mammalian cells. Molecular cloning techniques, such as PCR, were used to clone full length P53 and the mutations 248Q and 248W into pcDNA3.1. Cellular assays, such as MTT and cytotoxicity, were utilized in determining the effects of WT P53, R248Q, and R248W on MCF-7 cells. Preliminary results show that full length WT P53 decreases cell viability, while 248Q and 248W increase the MCF-7 viability. Further analysis is necessary to determine the effects of P53 mutants on DNA binding and cell proliferation.