Fig 2.

Role of NHE-1 in the control of energy metabolism, pH regulation and nude mice tumorigenicity. Tumour incidence in nude mice of the hamster lung cell lines derived from CCL39 cells. Parental hamster lung fibroblasts (wt), mutant cells impaired in respiration (res⁻), mutant cells impaired in glycolysis due to a lack of phosphoglucose isomerase activity (gly⁻), mutant cells lacking NHE-1 activity (nhe-1⁻) and mutant cells lacking both functions res⁻ nhe-1⁻ and gly⁻nhe-1⁻, were transformed with the H-ras oncogene and inoculated (1 × 10⁶ cells/mice) by subcutaneous injection into athymic nude mice. The combination of a defect in pHi regulation through mutation of nhe-1 (nhe-1⁻) or of high glycolysis (res⁻) resulted in transient tumour take (percentage of tumour bearing mice represented by dotted lines) but which regressed substantially. The full line shows the final tumour take. Combination of exacerbated glycolysis and a defect in pHi regulation through nhe-1 mutation (res⁻ nhe-1⁻) resulted rarely in tumour take.