In vitro interaction between human platelets and human neuroblastoma cells

W. De Matteis, S. Di Giulio, A. Menichelli, D. Del Principe, V. De Laurenzi, G. Melino

Research output: Contribution to journalArticlepeer-review

Abstract

The tumor microenvironment is important in determining the phenotypic stability of tumor cells. In fact zonal differences of growth factors, nutrients, stroma, oxygen, hormones as well as differentiation inducers or modulators and infiltrating host cells including platelets may play important roles in destabilising tumor cells and determining their susceptibilities to genetic and epigenetic changes. Moreover the interaction between platelets and tumor cells seems to be important for tumor metastasizing capacity. Abnormal haemostasis has also been noted in patients with neuroblastoma. We studied the effects of human neuroblastoma cells on platelet aggregation. Various neuroblastoma cell lines were tested but only SK-N-BE showed a significant alteration of platelet aggregation pattern. In fact this cell line inhibited human platelet aggregation induced by thrombin. Tumor cell supernatants did not affect aggregation significantly. Dead cells had a much lower inhibiting capacity. We also investigated the effect of platelets on neuroblastoma cells growth pattern. The results showed a moderate inhibition (around 20%) of tumor growth; even though occasionally under the same experimental conditions, platelets were able to enhance tumor growth (by around 100%). This biphasic effect may be explained in terms of balanced release of enhancing (PDGF, thromboxanes, etc. ) or inhibiting (PGD, arachidonic acid metabolites, etc.) factors by platelets. Further evidence for the interaction between platelets and neuroblastoma cells comes from the fact that platelets inhibit the fluorescence of neuroblastoma cells preloaded with dichlorofluorescin diacetate. In conclusion neuroblastoma cells inhibit platelet aggregation and their growth may be affected by platelets. These results seem relevant in understanding the bone marrow metastazing capacity of neuroblastoma tumor.

Original languageEnglish
Pages (from-to)337-343
Number of pages7
JournalClinical Chemistry and Enzymology Communications
Volume2
Issue number4-6
Publication statusPublished - 1990

ASJC Scopus subject areas

  • Clinical Biochemistry

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