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Cytosolic 5'-Nucleotidase II Silencing in a Human Lung Carcinoma Cell Line Opposes Cancer Phenotype with a

Rossana Pesi1, Edoardo Petrotto2, Laura Colombaioni3

  • 1Unità di Biochimica, Dipartimento di Biologia, Università di Pisa, Via San Zeno 51, 56127 Pisa, Italy. rossana.pesi@unipi.it.

International Journal of Molecular Sciences
|July 25, 2018
PubMed

Insights

Cytosolic 5'-nucleotidase II (cN-II) regulates purine metabolism. Inhibiting cN-II in cancer cells reduces proliferation and migration, suggesting potential therapeutic strategies.

Area of Science:

  • Biochemistry
  • Cancer Biology
  • Molecular Cell Biology

Background:

  • Purine homeostasis is crucial for cellular function, regulated by enzymes like cytosolic 5 extquotesingle-nucleotidase II (cN-II).
  • Elevated cN-II expression is linked to poor prognosis and chemoresistance in hematological malignancies, driving interest in cN-II inhibitors as cancer therapeutics.

Purpose of the Study:

  • To investigate the role of cN-II in cancer cell biology using a lung carcinoma cell line (A549) model.
  • To explore the effects of cN-II inhibition on cellular metabolism, proliferation, and viability.

Main Methods:

  • Partial silencing of cN-II in A549 cells and stabilization of its low-activity conformation using 2-deoxyglucose.
  • Analysis of nucleotide content, glutathione levels, glycolytic and Krebs cycle enzyme activities, protein synthesis, mitochondrial function, proliferation, migration, and viability.
  • Assessment of p53 phosphorylation status.

Main Results:

  • High cN-II expression correlated with a glycolytic, highly proliferative phenotype.
  • cN-II silencing led to reduced proliferation, protein synthesis, and migration, coupled with enhanced oxidative performance.
  • Similar effects were observed in a human astrocytoma cell line, and cN-II silencing was associated with p53 phosphorylation.

Conclusions:

  • cN-II plays a significant role in promoting a proliferative and glycolytic cancer cell phenotype.
  • Inhibition of cN-II activity may represent a viable strategy for cancer therapy, potentially by shifting cellular metabolism towards oxidative pathways and impacting proliferation.
  • The p53 pathway may be involved in mediating the cellular effects of cN-II inhibition.
Keywords:
2-deoxyglucoseCytosolic 5′-nucleotidasecell proliferationhuman lung carcinomap53

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