6533b7cffe1ef96bd1258464

RESEARCH PRODUCT

Different immunohistochemical levels of Hsp60 and Hsp70 in a subset of brain tumors and putative role of Hsp60 in neuroepithelial tumorigenesis

E. UntiFrancesco CappelloNunzia ScibettaPierpaolo BaiamonteFrancesca Rappa

subject

AdultMalePathologymedicine.medical_specialtyanimal structuresHistologyAdolescentNeuroepithelial CellsBiophysicschemical and pharmacologic phenomenaBiologymedulloblastomamedicine.disease_causemeningiomacomplex mixturesHsp60 Hsp70 astrocytoma glioblastoma multiformae medulloblastoma meningiomaHsp70Meningeal NeoplasmsmedicineHumansHSP70 Heat-Shock ProteinsMeningeal NeoplasmChildastrocytomalcsh:QH301-705.5AgedAged 80 and overMedulloblastomaHsp60 Hsp70 astrocytoma glioblastoma multiformae medulloblastoma meningioma.Brain NeoplasmsBrief ReportfungiAstrocytomaChaperonin 60Cell BiologyMiddle AgedHsp60medicine.diseaseImmunohistochemistryNeoplasms NeuroepithelialNeuroepithelial cellglioblastoma multiformaelcsh:Biology (General)Tumor progressionChild PreschoolCancer cellImmunohistochemistryFemaleCarcinogenesis

description

In this work we analysed, by immunohistochemistry, a series of brain tumors to detect the levels and cellular distribution of Hsp60 and Hsp70. We found that Hsp60 levels were significantly higher than those of Hsp70 in neuroepithelial tumors, while levels of both molecules were not significantly different from each other in meningeal neoplasms. In particular, Hsp60 immunopositivity was present mainly at the cytoplasmic level, while Hsp70 immunopositivity was found both in the cytoplasm and in the nucleus of tumor cells. The levels of these molecules in healthy control cells were always very low. Finally, Hsp60 and Hsp70 levels did not correlate with the different types (WHO grade) of neoplasm. Our results are partially in agreement with previous studies and suggest that Hsp60 is not increased by a passive phenomenon (e.g., due to the stress caused by the peritumor environment on cancer cells) but may be actively implicated in tumor progression, e.g. inhibiting tumor cell death or antitumor immune system response, as already postulated in vitro. We also briefly discuss the most recent publications on the extramitochondrial localization of Hsp60 in tumor cells and its role in tumor progression.

https://doi.org/10.4081/ejh.2013.e20