Table 1 The effect of individual statins on viability, cell penetrance, and gene expression in MiaPaCa-2 pancreatic cancer cells.

IC₅₀ studies* [24 h exposure, μM]		Gene expression studies	Upregulated genes (No.)	Downregulated genes (No.)	Total genes with changed expression (No.)	i.c. concentration of statin [nmol/100 000 cells]**		Proportion of i.c. statin concentration to that of lovastatin [%]	Lipophilicity of statins***
Cerivastatin	10	Cerivastatin	397	268	665	Lovastatin	301.1	—	Atorvastatin
Simvastatin	12	Pitavastatin	344	320	664	Fluvastatin	189.1	97	Simvastatin
Lovastatin	13	Simvastatin	128	38	166	Simvastatin	156.4	61	Pitavastatin
Pitavastatin	20	Fluvastatin	59	15	74	Cerivastatin	146.3	56	Cerivastatin
Fluvastatin	26	Atorvastatin	41	10	51	Atorvastatin	111.5	52	Fluvastatin
Atorvastatin	27	Lovastatin	33	5	38	Pitavastatin	92.6	36	Lovastatin
Pravastatin	29	Pravastatin	0	0	0	Pravastatin	50.7	25	Pravastatin
Rosuvastatin	36	Rosuvastatin	0	0	0	Rosuvastatin	26.6	18	Rosuvastatin

*Data retrieved from¹³ were combined with those of pitavastatin experiment.
**i.c. statin concentration measured at the end of 24-h incubation and recalculated to 100 000 cells to take into account different antiproliferative potential of individual statins.
***Statins sorted from the most to the least lipophilic compounds. Lipophilicity of ring-opened forms of statins based on partition between n-octanol and water⁵¹.
Analyses of intracellular (i.c.) concentrations of statins were performed in duplicates after 24 h incubation with respective statin (initial concentration was 12 μM).
Differentially transcribed genes detected in statin-treated cells (12 μM) compared to untreated control samples. Presented are only the transcripts with FC > 2.0 or < 0.5 and FDR < 0.05 (FC – fold change, FDR – false discovery rate). For full list of differentially regulated transcripts see the ArrayExpress database, accession E-MTAB-3979.

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