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Nucleoside diphosphate kinase (NDPK/NM23) and the waltz with multiple partners: possible consequences in tumor

D Roymans1, R Willems, D R Van Blockstaele

  • 1Department of Biomedical Sciences, University of Antwerp, Antwerpen, Belgium.

Clinical & Experimental Metastasis
|October 31, 2002
PubMed

Insights

Nucleoside diphosphate kinases (NDPKs), encoded by the NM23 gene family, are implicated in cancer metastasis. Protein-NDPK interactions are crucial for modulating NDPK functions in tumor progression and metastasis.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Tumor metastasis is a primary cause of cancer mortality.
  • The NM23 gene family encodes nucleoside diphosphate kinases (NDPKs), which are implicated in tumor metastasis.
  • NDPKs possess phosphotransferase activity but also exhibit other functions, including transcriptional regulation and protein kinase activity.

Purpose of the Study:

  • To review the correlation between NDPKs and cancer.
  • To discuss the mechanisms by which NDPK activities influence metastasis.
  • To emphasize the role of protein-NDPK interactions in cancer metastasis.

Main Methods:

  • Literature review of studies on NM23/NDPKs in cancer metastasis.
  • Analysis of reported NDPK functions beyond phosphotransferase activity.
  • Examination of identified NDPK binding partners and protein-protein interactions.

Main Results:

  • Eight human NM23 isoforms (NDPKs) have been identified.
  • NDPKs' role in metastasis extends beyond phosphotransferase activity.
  • Protein-protein interactions significantly modulate NDPK functions in metastasis.

Conclusions:

  • NDPKs are critical regulators of cancer metastasis.
  • Understanding protein-NDPK interactions is key to deciphering NDPK roles in cancer progression.
  • Targeting protein-NDPK interactions may offer novel therapeutic strategies for cancer metastasis.

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