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To clarify the changes of gene expression in the process of acquired resistance, we established seven gemcitabine-resistant subclones of the PCI43, PK1, and KLM1 cell lines.
As shown in Figure 4, the ratio of hENT1 × dCK/ RRM1 × RRM2 expression progressively decreased in the process of acquired gemcitabine resistance.
Among these, AS participates in the process of acquired chemoresistance by controlling the expression of cancer-related splice variants that contribute to cancerous phenotype.
Understanding alterations in expression of genes, which characterise the response of cancer cells to gemcitabine treatment in the process of acquired resistance, would allow us to improve therapeutic strategies for pancreatic cancer.
Although it has been proposed that the genes for gemcitabine transport and metabolism are involved in the mechanism of cellular resistance to gemcitabine, it is not fully understood how gemcitabine influences its own transport and metabolism in the process of acquired resistance.
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