BACKGROUND: Hyaluronidase is hypothesised to play a role in cancer invasion and metastasis formation. MATERIALS AND METHODS: Hyaluronidase activity was investigated at pH 3.8 in extracts of 30 human brain tumours (17 glioblastomas and 13 brain metastases of carcinomas) and in cancer cell cultures with the ELSA method and zymography. RESULTS: In brain metastases, hyaluronidase activities were significantly higher than in glioma extracts (9.16 +/- 4.48 mU/g vs 4.25 +/- 5.74) which was not explained by serum hyaluronidase contamination. Serum hyaluronidase of tumour patients' sera was within the normal values determined in 28 matched blood donors'sera (33.8 +/- 11 U/l). The maximum hyaluronidase/albumin (U/g) ratio was 0.9, below which the hyaluronidase content of tumours was below the maximum value calculated from the albumin content of the tumour extract and could not be considered as local production by tumour cells. The hyaluronidase content and hyaluronidase/albumin ratio of metastasis extracts was significantly higher than in glioma extracts and patients' sera, whereas no significant difference was found between the ratios of glioma extracts and sera. The production of hyaluronidase was studied in cell extracts and in culture media of 3 human glioma-derived cell lines and of the brain metastasis-derived cell line SA87. Hyaluronidase activity of the metastasis-derived cell line SA87 was 100 to 1000-fold that of glioma cell lines. CONCLUSION: These results suggest that hyaluronidase is associated with the more aggressive cancer cells and is directly or indirectly involved in brain metastasis phenotype.
BACKGROUND: Hyaluronidase is hypothesised to play a role in cancer invasion and metastasis formation. MATERIALS AND METHODS: Hyaluronidase activity was investigated at pH 3.8 in extracts of 30 humanbrain tumours (17 glioblastomas and 13 brain metastases of carcinomas) and in cancer cell cultures with the ELSA method and zymography. RESULTS: In brain metastases, hyaluronidase activities were significantly higher than in glioma extracts (9.16 +/- 4.48 mU/g vs 4.25 +/- 5.74) which was not explained by serum hyaluronidase contamination. Serum hyaluronidase of tumourpatients' sera was within the normal values determined in 28 matched blood donors'sera (33.8 +/- 11 U/l). The maximum hyaluronidase/albumin (U/g) ratio was 0.9, below which the hyaluronidase content of tumours was below the maximum value calculated from the albumin content of the tumour extract and could not be considered as local production by tumour cells. The hyaluronidase content and hyaluronidase/albumin ratio of metastasis extracts was significantly higher than in glioma extracts and patients' sera, whereas no significant difference was found between the ratios of glioma extracts and sera. The production of hyaluronidase was studied in cell extracts and in culture media of 3 humanglioma-derived cell lines and of the brain metastasis-derived cell line SA87. Hyaluronidase activity of the metastasis-derived cell line SA87 was 100 to 1000-fold that of glioma cell lines. CONCLUSION: These results suggest that hyaluronidase is associated with the more aggressive cancer cells and is directly or indirectly involved in brain metastasis phenotype.
Authors: Alamelu G Bharadwaj; Joy L Kovar; Eileen Loughman; Christian Elowsky; Gregory G Oakley; Melanie A Simpson Journal: Am J Pathol Date: 2009-02-13 Impact factor: 4.307