Cervical cancer metabolism: Major reprogramming of metabolic pathways and cellular energy production

Abstract

Abstract A few important changes in tumor cellular bioenergetics include elevated glycolysis, enhanced glutaminolytic flux, amino acid upregulation and lipid metabolism, mitochondrial biogenesis development, pentose phosphate pathway (PPP) stimulation, and biosynthesis of macromolecules. Cervical cancer (CC) cells are also found to reprogram cellular metabolic pathways. Cancer cells are benefitted due to increased hexokinase 2 expression by providing metabolites for growth, supplying intermediates for tricarboxylic acid, assisting autophagy in response to deprivation of glucose, and binding to voltage-dependent anion channel. Oncogenic signals like protein kinase B mechanistic target of rapamycin-related pathways were found to be activated by human papillomavirus (HPV) E6/E7 and they have put out the action of p53 and pRb tumor-suppressive paths, suggesting that HPV E6/E7 could regulate cellular glucose breakdown of CC. Variations in cancer cells’ metabolism are related with overexpression of oncogenes (c-Myc) and transcription factors (hypoxia inducible factor 1a). The expression of 6-phospho glyceraldehyde dehydrogenase and PPP activity to phosphorylation of c-MET is being investigated. It is also known that CC cells can turn out lipoprotein A under certain conditions. Metabolic reprogramming also aids in therapeutic interventions. For cervical and other cancers, the maximum standardized uptake value is an additional prognostic marker along with lymph node grade, cancer stage, and tumor size.