Abstract
Tumor cells exhibit rewired metabolism. We carried out comparative analyses attempting to investigate whether metabolic reprograming could be measured by isothermal microcalorimetry. Intact metastatic cell lines of tongue cell carcinoma, human and murine melanoma, lung, and breast tumors consistently released more heat than non-metastatic cells or cells displaying lower metastatic potential. In tongue squamous carcinoma cells mitochondrial enriched extract reproduced the heat release pattern of intact cells. Cytochalasin D, an actin filament inhibitor, and suppression of metastasis marker Melanoma associated gene 10 (MAGEA10) decreased heat release. Uncoupling protein 2 was highly expressed in metastatic cells, but not in non-metastatic cells. Carnitine palmitoyl transferase-1 inhibitor, Etomoxir strongly inhibited heat release by metastatic cells, thus linking lipid metabolism to thermogenesis. We propose that heat release may be a quantifiable trait of the metastatic process.
Highlights
Evidence has accumulated to show convincingly that the metabolism of tumor cells differs significantly from that of the majority of normal cells
The total heat output reflected higher rates of heat release as shown in Supplementary Figure 2. These results show that heat release by the different cell lines as measured at 5 min intervals was constant over time displaying clearly distinct slopes
In LN-2 shMAGEA10 cells, there was a reduction of more than 50% in the mRNA expression of uncoupling protein 2 (UCP2), again corroborating the results shown in Figures 2, 3 and reinforcing the hypothesis that adhesive/motility properties of LN-2 cells may be connected to heat dissipation
Summary
Evidence has accumulated to show convincingly that the metabolism of tumor cells differs significantly from that of the majority of normal cells. Irrespective of the multiple alterations contributing to the so-called metabolic reprogramming, it is generally agreed that the major differences implicate the glycolytic and the tricarboxylic cycle pathways coupled to the oxidative phosphorylation (OXPHOS) system [1, 2]. This is not surprising in view of the roles played by these pathways as the principal suppliers of ATP for tumor cells. In this context tumor cells are broadly classified according to the prevailing type of metabolism i.e., glycolytic or oxidative.
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