Pyruvate kinase type M2: A key regulator of the metabolic budget system in tumor cells

摘要: Cell proliferation only proceeds when metabolism is capable of providing a budget metabolic intermediates that adequate to ensure both energy regeneration and the synthesis cell building blocks in sufficient amounts. In tumor cells, glycolytic pyruvate kinase isoenzyme M2 (PKM2, M2-PK) determines whether glucose converted lactate for (active tetrameric form, Warburg effect) or used (nearly inactive dimeric form). This review discusses regulation mechanisms expression by different transcription factors as well activity direct interaction with certain oncoproteins, tyrosine serine phosphorylation, binding phosphotyrosine peptides, association other non enzymes, promyelocytic leukemia suppressor protein, intermediates. An intervention expression, tetramer dimer ratio has severe consequences tumorigenic capacity cells which makes this enzyme promising target potential therapeutic approaches. The quantification form (Tumor plasma stool allows early detection tumors therapy control. Several may induce translocation into nucleus. role nucleus complex witnessed evidence its effect pro-proliferative pro-apoptotic stimuli.