Cancer chemotherapy resistance (MDR) is the innate and/or acquired ability of cancer cells to evade the effects of chemotherapeutics and is one of the most pressing major dilemmas in cancer therapy. Chemotherapy resistance can arise due to several host or tumor-related factors. However, most current research is focused on tumor-specific factors and specifically genes that handle expression of pumps that efflux accumulated drugs inside malignantly transformed types of cells. In this work, we suggest a wider and alternative perspective that sets the stage for a future platform in modifying drug resistance with respect to the treatment of cancer.

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The Na(+)/H(+) exchanger isoform 1 (NHE1) is a ubiquitously expressed transporter fulfilling a variety of cell physiological tasks. By importing Na(+) and exporting H(+), NHE1 contributes to regulatory volume increase and cytoplasmic pH homeostasis. In addition it anchors the cytoskeleton in the plasma membrane. NHE1 plays a critical role in mediating the progression of reperfusion injuries after ischemia. Moreover, it is upregulated and/or overexpressed in a number of tumour cells. In many cases an elevated NHE1 activity can be correlated with an increase in cell motility and malignancy. Consequently, NHE1 including its regulators may represent potential targets in anticancer therapy. Different NHE1 inhibitors are compared and possible clinical exploitations of NHE1 inhibition are discussed.