Preliminary Investigation into the Effects of Nicotine on Urinary Bladder Cancer Cell Lines

Maria Rechtin Thomas More College, Nick Auteri Thomas More College, Kyle Damen College of Mount St. Joseph, Laura Felix Thomas More College, Taylor Schnebelt Xavier University, Avery Henderson Thomas More College, Rachel Bender Capital University, Evan Birmingham University of Dayton, Alex White Miami University of Ohio, Alexandra Wright University of Louisville
Faculty Sponsor(s): Julia Carter Not Affiliated with a College/University, Bonnie Richmond Not Affiliated with a College/University
Throughout history, cancer has plagued mankind, and with the number of diagnoses growing in past centuries, it is now the plague of the modern era. Still, many cancers are under researched and under funded, including bladder cancer, with the act of cigarette smoking increasing the risk of bladder cancer four fold. In most cases, the intake of nicotine occurs via cigarettes, containing approximately 75 known carcinogens. While not carcinogenic, nicotine is classified as a promoter of carcinogenesis. Chemicals, such as nicotine, filter though the kidney into the urine, and subsequently are exposed to the bladder epithelium. The goal of this study was to examine the effects of nicotine exposure on urinary bladder cancer cells of varying grades. Five cell lines, ATCC-HTB-2 [RT4] (grade 0), ATCC-HTB-4 [T-24] (grade 1), ATCC-HTB-9 [5637] (grade 2), ATCC-CRL-1472 [HT-1376] (grade 3), and ATCC-HTB-5 [TCCSUP] (grade 4), were studied. Results of viability and proliferation assays suggest no correlation between tumor grade and viability or proliferation. It was observed that ATCC-HTB-9 [5637] cells require two days for media conditioning prior to growth. p38 MAP kinase, a protein associated with cellular proliferation, survival, and apoptosis, eukaryotic initiation factor 4e (eIF4E), a protein associated with protein translation, and the alpha-7 nicotinic receptor, a subunit of the nicotinic acid receptor, were examined. Decreased expression of eIF4E was observed in T-24 cells, however, p38 MAP kinase and alpha-7 nicotinic receptors were equally expressed. Understanding the influence of nicotine on these proteins may contribute to the development of future chemotherapeutic drugs.
Oral Presentation

When & Where

10:45 AM
Gallahue Hall 102