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Editorial
. 2024 May 22:15:1390877.
doi: 10.3389/fendo.2024.1390877. eCollection 2024.

Editorial: Altered metabolic traits in gastrointestinal tract cancers

Seema Parte  1 , Ramesh Pothuraju  2 , Ranjith Kumavath  3 , Rakesh Bhatia  1   4 , Rama Krishna Nimmakayala  5 , Shailendra Gautam  1   6
Affiliations
Editorial

Editorial: Altered metabolic traits in gastrointestinal tract cancers

Seema Parte et al. Front Endocrinol (Lausanne). .
No abstract available

Keywords: gastro-intestinal tract cancers; glycolysis; lipid metabolism; metabolic targeting; oncogenic and metabolic signaling; tumor metabolism.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Figures

Figure 1
Figure 1
Schematic representation of metabolic hubs that synchronize with key oncogenic/tumor suppressor gene signaling cascades in cancer: The complex interplay of aerobic glycolysis, glutamine metabolism and lipid (fatty acid) metabolism forms a complex repertoire that in turn crosstalks with major oncogenic/tumor suppressor genes and other signaling pathways (Kras, c-myc, p53, mTOR, JAK/STAT3, Wnt etc.) to influence oxidative phosphorylation (OXPHOS), ATP turnover, ROS production, gene transcription etc., and ultimately mitochondrial bioenergetics. Tumor cells with impaired receptor tyrosine kinases (RTKs) reveal altered downstream cellular respiration and signal transduction. Such altered tumor cells may communicate with other cells in their vicinity i.e. the tumor microenvironment (TME i.e. stromal cells, immune cells etc.) during tumor initiation and progression thus complicating their pathophysiology. Oncogenic signaling hubs are indicated in green. Targeting of these RTKs with an antibody-based approach and small-molecule inhibition demonstrate potential targets for onco-therapy. Dotted portions of lines indicate overlap of the arrows, red bars indicate inhibition. ACC: acetyl CoA carboxylase, ACLY: ATP citrate lyase, ADP-Adenosine diphosphate, AMPK: AMP-activated protein kinase, EGF: Epidermal growth factor, FASN: fatty acid synthase, bisP: bisphosphate, GF: growth factor, G1-P: Glucose 1-phosphate, 6P-6-phosphate, GLUT: Glucose transporter, HKII- Hexokinase 2, LDHA-Lactate dehydrogenase A, MAB EC domain: Monoclonal antibody extracellular domain, NADP/NADPH: Nicotinamide adenine dinucleotide phosphate, OAA: Oxaloacetate, PDH: Pyruvate dehydrogenase, PDK1: Pyruvate dehydrogenase kinase 1, PEP: Phosphoenolpyruvate, PKM1, 2-Pyruvate kinase, PPP: Pentose phosphate pathway, ROS: Reactive oxygen species, RTKs: Receptor tyrosine kinases, SLC1A5: solute carrier family 1 member 5, SMI-Small molecule inhibitor, TCA-Tricarboxylic Acid Cycle, TIGAR: TP53-inducible glycolysis and apoptosis regulator..
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