Investigating the Role of PA28γ in Early Carcinogenisis

Emily Aller, Michelle Ramirez, Alex Fusco, and Dr. Lance Barton, Department of Biology, Austin College, 900 N Grand Ave Sherman, TX 75090

Cancers are characterized by the accumulation of mutations, which contribute to an altered biology. The signaling circuits responsible for cancerous phenotypes vary from one cancer to the next, but evidence suggests that the protein PA28γ may have a role in some of these circuits. Notably, mice that do not have PA28γ form fewer and smaller skin tumors than their wild-type counterparts when treated with a topical mutagen.  Further studies have indicated that PA28γ plays roles in the development of multiple hallmarks of cancer, including migration, excessive proliferation, and chromosomal instability, which indicate that PA28γ may be an important factor in the deregulation of cell circuitry and the development of cancer. 

This study sought to deepen the understanding of PA28γ’s role in the development of cancer by investigating how chemically transformed cells with and without the PA28γ gene compare to a variety of cancer cell lines with a range of PA28γ expression, including A9, M158, 4T1 and LL/2s. Scratch assays and Transwell Migration Assays were used to assess the migratory capability of each cell line, while flow cytometry was used to investigate their cell cycles and genetic instability. Additionally, genetic sequencing was used to identify any mutations in several common oncogenes and tumor suppressors including p53, Akt1, and H-Ras.  Overall, these data yielded evidence that chemically transformed cells display intermediate phenotypes between normal cells and cancer cells, without a distinguishable role for PA28γ. Consequently, future studies will focus on removing PA28γ expression from these cancer cell lines.

Additional Abstract Information

Presenters: Emily Aller, Michelle Ramirez

Institution: Austin College

Type: Poster

Subject: Biology

Status: Approved

Time and Location

Session: Poster 2
Date/Time: Mon 3:00pm-4:00pm
Session Number: 2658