Although sufficient evidence supports the antitumoral
function of melatonin in some tumor types [24], little is
known about the functional effects of this indolamine in
cancer cells expressing a stem cell-like phenotype and,
particularly, how that effect depends on mitochondrial
activity. In general, factors which allow melatonin to
recognize context specificity and induce apoptosis in some
types of cancer cells only are not completely known [24].
In the present study, we analyze the effect of melatonin
in the P19 CSCs model which allows testing the effect
of different molecules in distinct metabolic contexts and
stemness stages. Interestingly, we found that only cells
relying on a more oxidative metabolism for ATP production
were susceptible to melatonin. Thus, this work aims the
understanding of the mechanisms that make these cells
vulnerable to melatonin in comparison with their glycolytic
counterparts.
Although sufficient evidence supports the antitumoralfunction of melatonin in some tumor types [24], little isknown about the functional effects of this indolamine incancer cells expressing a stem cell-like phenotype and,particularly, how that effect depends on mitochondrialactivity. In general, factors which allow melatonin torecognize context specificity and induce apoptosis in sometypes of cancer cells only are not completely known [24].In the present study, we analyze the effect of melatoninin the P19 CSCs model which allows testing the effectof different molecules in distinct metabolic contexts andstemness stages. Interestingly, we found that only cellsrelying on a more oxidative metabolism for ATP productionwere susceptible to melatonin. Thus, this work aims theunderstanding of the mechanisms that make these cellsvulnerable to melatonin in comparison with their glycolyticcounterparts.
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