چکیده (انگلیسی):

Altered cellular metabolismis a fundamental adaptation of cancer during rapid proliferation as a result of growth
factor overstimulation. We review different pathways involving metabolic alterations in cancers including aerobic
glycolysis, pentose phosphate pathway, de novo fatty acid synthesis, and serine and glycine metabolism. Although
oncoproteins, c-MYC, HIF1α and p53 are the major drivers of this metabolic reprogramming, posttranscriptional
regulation by microRNAs (miR) also plays an important role in finely adjusting the requirement
of the key metabolic enzymes underlying this metabolic reprogramming. We also combine the literature data
on the miRNAs that potentially regulate 40 metabolic enzymes responsible for metabolic reprogramming in cancers,
with additional miRs fromcomputational prediction. Our analyses showthat: (1) a metabolic enzymeis frequently
regulated by multiple miRs, (2) confidence scores from prediction algorithms might be useful to help
narrowdown functional miR-mRNA interaction,which might be worth further experimental validation. By combining
known and predicted interactions of oncogenic transcription factors (TFs) (c-MYC, HIF1α and p53), sterol
regulatory element binding protein 1 (SREBP1), 40 metabolic enzymes, and regulatory miRs we have established
one of the first reference maps for miRs and oncogenic TFs that regulate metabolic reprogramming in cancers.
The combined network shows that glycolytic enzymes are linked to miRs via p53, c-MYC, HIF1α, whereas the
genes in serine, glycine and one carbon metabolism are regulated via the c-MYC, as well as other regulatory organization
that cannot be observed by investigating individual miRs, TFs, and target genes.