Increasing evidence witnesses that
cancer metabolism alterations represent a critical hallmark for many types of human
tumors. There is a strong need to understand and dissect the molecular mechanisms underlying
cancer metabolism to envisage specific
biomarkers and underpin critical molecular components that might represent novel therapeutic targets. One challenge, that is the focus of this review, is the reprogramming of the altered metabolism of a
cancer cell toward that of un-transformed cell. The anti-hyperglicemic agent,
metformin has proven to be effective in reprogramming the metabolism of
cancer cells even from those subpopulations endowed with
cancer stem like features and very high chemoresistenace to conventional anticancer treatments. A functional interplay involving selective modulation of
microRNAs (
miRNAs) takes place along the anticancer metabolic effects exerted by
metformin. The implications of this interplay will be also discussed in this review.