Investigating the effects of p53 mutations on cancer phenotypes in transformed MEF cells

• In Event: Poster Presentation and Judging for: Biomedical; Cell & Molecular Biology; Chemistry & Biochemistry; Marine Science; Systematics & Evolutionary Biology.
  In Poster Session: Cell & Molecular Biology Poster session

Abstract

Cancer is an accumulation of mutations in cells. Typically, cancers exhibit specific phenotypes known as the Hallmarks of Cancer; six hallmarks have been identified and include replicative immortality, invasion and metastasis. The protein p53 has a key role in numerous pathways that are known to contribute to these hallmarks. Four cell lines, control mouse embryonic fibroblasts (MEF), mutated mouse embryonic fibroblasts, or cancer clones (CC), carcinogenic mouse fibroblasts (A9), and carcinogenic mouse mammary cells (M158), were studied to understand how mutated p53 can manifest into cancer phenotypes. These lines were tested to characterize the CC line on the continuum of increasing tumorigenic capacity. All four cell types had a mutation in the p53 coding region, however the nature of the mutations varied. Upon investigation of cancer hallmarks such as genomic and genetic instability, invasion/metastasis potential, and resistance to cell death/pro-apoptotic signals, experimental results from karyotyping, gene sequencing, and migration assays favored the prediction that the CC cell line behaved more similarly to the MEF cell line, the precursor cell type to the transformation, than the carcinogenic A9 and M158 cell lines. This was true of genetic and genomic instability, and invasion/metastasis phenotypes. A single mutational event is unlikely to result in a fully formed cancer cell, but would rather require a series of mutational events to overwhelm the ability of cells to self-regulate.

Authors

• Janani Ramesh, Austin College

• Emily Bourcier, Austin College