Wild type and gain of function mutant TP53 can regulate the sensitivity of pancreatic cancer cells to chemotherapeutic drugs, EGFR/Ras/Raf/MEK, and PI3K/mTORC1/GSK-3 pathway inhibitors, nutraceuticals and alter metabolic properties

James A. McCubrey; Akshaya K. Meher; Shaw M. Akula; Stephen L. Abrams; Linda S. Steelman; Michelle M. LaHair; Richard A. Franklin; Alberto M. Martelli; Stefano Ratti; Lucio Cocco; Fulvio Barbaro; Przemys&#x142;aw Duda; Agnieszka Gizak

doi:doi:10.18632/aging.204038

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Research Paper Volume 14, Issue 8 pp 3365—3386

Wild type and gain of function mutant TP53 can regulate the sensitivity of pancreatic cancer cells to chemotherapeutic drugs, EGFR/Ras/Raf/MEK, and PI3K/mTORC1/GSK-3 pathway inhibitors, nutraceuticals and alter metabolic properties

Figure 8. Effects of pLXSN and WT-TP53 on clonogenicity in the presence of 5-Fluorouracil, gemcitabine or cisplatin in two PDAC cell lines. The clonogenicity in the presence of increasing concentrations of 5-fluorouracil (5FU), gemcitabine (Gem) and cisplatin (Cis) were examined in: MIA-PaCa-2 + pLXSN and MIA-PaCa-2 + WT-TP53 (A–C), PANC-28 + pLXSN, and PANC-28 + WT-TP53 (D–F). Red horizontal bars = MIA-PaCa-2 or PANC-28 containing pLXSN. Blue horizontal bars = MIA-PaCa-2 or PANC-28 containing WT-TP53. These experiments were repeated and similar results were observed. The colonies for each cell line were normalized to untreated so that the results from pLXSN and WT-TP53 could be compared. ^***P < 0.0001, ^**P < 0.005 and ^*P < 0.05.