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 12. Effects of pLXSN and WT-TP53 on the colony formation in soft agar in the presence of doxorubicin, verapamil and vismodegib. The effects of pLXSN and WT-TP53 on the colony formation in soft agar in MIA-PaCa-2 in response to drugs was examined. (A) Colony formation abilities of MIA-PaCa-2 + pLXSN (red bars) and MIA-PaCa-2 + WT-TP53 (blue bars) were compared in response to treatment with doxorubicin. (B) Colony formation abilities of MIA-PaCa-2 + pLXSN (red bars) and MIA-PaCa-2 + WT-TP53 (blue bars) were compared in response to verapamil. (C) Colony formation abilities of MIA-PaCa-2 + pLXSN (red bars) and MIA-PaCa-2 + WT-TP53 (blue bars) were compared in response to treatment with vismodegib. The number of colonies for each cell line were normalized to untreated so that the results from pLXSN and WT-TP53 could be compared. These studies were repeated and similar results were observed. ^***P < 0.0001, and ^**P < 0.005.