Nm23-H1 promotes adhesion of CAL 27 cells in vitro.

Mol Carcinog

Rudjer Boskovic Institute, Division of Molecular Medicine, Laboratory for Molecular Oncology, 10 002 Zagreb, Croatia.

Published: September 2009

AI Article Synopsis

  • Nm23-H1 is identified as a metastatic suppressor gene that reduces the metastatic potential in carcinoma cell lines but its exact mechanism of action remains unclear.
  • Research focused on CAL 27 cells (oral squamous cell carcinoma) showed that those overexpressing nm23-H1 had lower migratory and invasive abilities and exhibited stronger adhesion on certain substrates.
  • Findings indicate that nm23-H1 enhances cell adhesion without disrupting EGF-induced Ras signaling, providing insights into its role in regulating cell behavior in cancer.

Article Abstract

nm23-H1 was found to diminish metastatic potential of carcinoma cell lines and therefore was placed in the group of metastatic suppressor genes. Its protein product has a function of a nucleoside diphosphate kinase (NDPK) as well as protein kinase and nuclease. Though it was found that Nm23-H1 is involved in many cellular processes, it is still not known how it promotes metastatic suppressor activity. Since the process of metastasis is dependent on adhesion properties of cells, the goal of our work was to describe the adhesion properties of CAL 27 cells (oral squamous cell carcinoma of the tongue) overexpressing FLAG/nm23-H1. In our experiments, cells overexpressing nm23-H1 show reduced migratory and invasive potential. Additionally, cells overexpressing nm23-H1 adhere stronger on substrates (collagen IV and fibronectin) and show more spread morphology than the control cells. Results obtained by EGF induction of migration revealed that the adhesion strength predetermined cell response to chemoattractant and that Nm23-H1, in this cell type, does not interfere with, EGF induced, Ras signaling pathway. These data contribute to the overall knowledge about nm23-H1 and its role in cell adhesion, migration, and invasion, especially in oral squamous cell carcinoma.

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Source
http://dx.doi.org/10.1002/mc.20536DOI Listing

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