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pH Regulatory Transporters in Pancreatic Ductal Adenocarcinoma (PDAC)

PDAC is among the most aggressive human malignacies, with a 5‐ year survival rate of 1–4%. Elucidation of specific molecular alterations in PDAC is urgently needed to devise new treatment strategies. Malignant tumors with rapid progression such as PDAC often undergo extensive metabolic changes resulting in increased acid production. We and others have shown in other cancers that this leads to the upregulation of acid extruding transporters, which in turn favors further cancer progression. The aim of our studies is to elucidate the regulation and roles of pH regulatory ion transporters in PDAC. We used qPCR to screen a panel of 4 human PDAC cell lines (AsPC‐1, BxPC‐3, Panc‐1, MIAPaCa‐2) against a normal human pancreatic ductal cell line (HPDE). The Na+/H+ exchanger 2 (NHE2) was upregulated in 3 of 4 cell lines, whereas NHE1 was upregulated only in BxPC3 cells; the V‐type H+‐ATPase subunit a3 was upregulated in all PDAC cell lines; all cell lines except BxPC3 exhibited upregulation of either AE2 or AE3 Cl−/HCO3−exchangers, and also the Na+‐HCO3− transporters SLC4A7 and –A8 tended to be upregulated in PDAC; surprisingly, the H+/lactate cotransporter MCT1 was downregulated in all PDAC cell lines and a similar trend was seen for MCT4. In conclusion, PDAC cell lines exhibit dramatic changes in the mRNA expression level of pH‐regulatory transporters. Ongoing experiments are addressing the functional relevance of this in PDAC.