Multifaceted entrancing role of glucose and its analogue, 2-deoxy-D-glucose in cancer cell proliferation, inflammation, and virus infection.
Level 5 - mechanism / opinion, no new human data
Narrative review detailing mechanistic pathways without primary clinical data
PubMed 36228369 · doi:10.1016/j.biopha.2022.113801
What was done
This narrative review summarizes molecular mechanisms through which chronic hyperglycemia drives cancer progression, systemic inflammation, and susceptibility to viral infections, while evaluating the therapeutic mechanisms of the glucose analogue 2-deoxy-D-glucose (2-DG).
What was found
The abstract provides a descriptive overview of molecular mechanisms and reports no numerical data or effect sizes. It details that high glucose activates oncogenic pathways (PI3K, Akt, mTOR, Ras, Raf, MAPK, PKC), stabilizes HIF-1α, promotes reactive oxygen species and advanced glycation end-products, and increases pro-inflammatory mediators. In contrast, 2-DG enters cells via GLUT transporters, is phosphorylated to 2-DG-6-phosphate, inhibits glycolysis, the TCA cycle, and the pentose phosphate pathway, causes ATP depletion, activates AMPK and SIRT-4, and suppresses viral replication and inflammatory signaling.
Why it matters
The review outlines how targeting cellular glucose metabolism with 2-DG may offer broad therapeutic utility across oncologic, inflammatory, and infectious disease contexts.
Limits
The abstract contains no primary experimental or clinical data, no systematic search methodology, and no quantitative metrics. The presented mechanisms rely largely on preclinical and theoretical models with unquantified clinical translation.
Cited by
- supports 2-deoxyglucose is taken up by cells like glucose, cannot be metabolized to produce ATP, and competitively inhibits hexokinase.