Skip to main content
Log in

PFKP phenotype in lung cancer: prognostic potential and beyond

  • Short Communication
  • Published:
Molecular Biology Reports Aims and scope Submit manuscript

Abstract

Rapid utilization of glucose is a functional marker of cancer cells, and has been exploited in the clinical diagnosis of malignancies using imaging technology. Biochemically, an increase in the rate of glycolysis, (i.e.) the process of conversion of glucose into pyruvate accelerates the net rate of glucose consumption. One of the critical determinants of glycolytic flux is the enzyme, phosphofructokinase (PFK) which converts fructose-6-phosphate into fructose 1,6, bisphosphate. PFK activity is allosterically inhibited or upregulated by cellular ATP or AMP, respectively. In a recent report of Cellular Oncology, Shen et al., have investigated one of the forms of PFK known as the platelet-type PFK (PFKP) in lung cancer. Using clinical samples as well as experimental models the authors unravel the cancer-related roles of PFKP and demonstrate that PFKP phenotype may predict the prognosis of lung cancer. In this letter, the findings are discussed in the light of recent research to expand the potential application and clinical impact of PFKP phenotype in lung cancer.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

References

  1. Shen J, Jin Z, Lv H, Jin K, Jonas K, Zhu C, Chen B (2020) PFKP is highly expressed in lung cancer and regulates glucose metabolism. Cell Oncol (Dordrecht) 43:617–629

    Article  CAS  Google Scholar 

  2. Ganapathy-Kanniappan S, Geschwind JF (2013) Tumor glycolysis as a target for cancer therapy: progress and prospects. Mol Cancer 12:152

    Article  Google Scholar 

  3. Liberti MV, Dai Z, Wardell SE, Baccile JA, Liu X, Gao X, Baldi R, Mehrmohamadi M, Johnson MO, Madhukar NS, Shestov AA, Chio IIC, Elemento O, Rathmell JC, Schroeder FC, McDonnell DP, Locasale JW (2017) A predictive model for selective targeting of the warburg effect through GAPDH inhibition with a natural product. Cell Metab 26:648–659.e8

    Article  CAS  Google Scholar 

  4. Alam H, Tang M, Maitituoheti M, Dhar SS, Kumar M, Han CY, Ambati CR, Amin SB, Gu B, Chen TY, Lin YH, Chen J, Muller FL, Putluri N, Flores ER, DeMayo FJ, Baseler L, Rai K, Lee MG (2020) KMT2D deficiency impairs super-enhancers to confer a glycolytic vulnerability in lung cancer. Cancer Cell 37:599–617.e7

    Article  CAS  Google Scholar 

  5. Park JS, Burckhardt CJ, Lazcano R, Solis LM, Isogai T, Li L, Chen CS, Gao B, Minna JD, Bachoo R, DeBerardinis RJ, Danuser G (2020) Mechanical regulation of glycolysis via cytoskeleton architecture. Nature 578:621–626

    Article  CAS  Google Scholar 

  6. Tang H, Lee M, Sharpe O, Salamone L, Noonan EJ, Hoang CD, Levine S, Robinson WH, Shrager JB (2012) Oxidative stress-responsive microRNA-320 regulates glycolysis in diverse biological systems. FASEB J 26:4710–4721

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Shanmugasundaram Ganapathy-Kanniappan.

Ethics declarations

Conflict of interest

The author declares that there is no conflict of interest.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Ganapathy-Kanniappan, S. PFKP phenotype in lung cancer: prognostic potential and beyond. Mol Biol Rep 47, 8271–8272 (2020). https://doi.org/10.1007/s11033-020-05805-9

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s11033-020-05805-9

Keywords

Navigation