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Troglitazione affects survival of human osteosarcoma cells
Author(s) -
Lucarelli Enrico,
Sangiorgi Luca,
Maini Veronica,
Lattanzi Giovanna,
Marmiroli Sandra,
Reggiani Matteo,
Mordenti Marina,
Gobbi Giuliana Alessandra,
Scrimieri Francesca,
Zambon Bertoja Annarosa,
Picci Piero
Publication year - 2002
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.10203
Subject(s) - apoptosis , cell growth , protein kinase b , troglitazone , osteosarcoma , cell culture , cancer research , mtt assay , mediator , biology , receptor , programmed cell death , peroxisome proliferator activated receptor , microbiology and biotechnology , endocrinology , medicine , biochemistry , genetics
Activation of PPARγ, a transcription factor member of the family of peroxisome proliferator‐activated receptors, induces apoptosis in several normal and tumor cell lines. In our study, we investigated whether treatment with troglitazone (TRO), a known PPARγ agonist, induced apoptosis in the human osteosarcoma (OS) cell lines G292, MG63, SAOS and U2OS that express PPARγ. In our experiments, TRO never induced apoptosis of OS cells; on the contrary, TRO increased cell number, based on MTT proliferation assay. Remarkably, the TRO‐induced cell number increase depended on a decrease of apoptosis that naturally occurred in the culture and was not due to an increased cell proliferation rate. TRO also prevented staurosporin‐induced apoptosis. The TRO‐mediated survival effect correlated with the activation of Akt, a well‐known mediator of survival stimuli. Our work describes a new function for TRO and indicates that the Akt survival pathway may be a mediator of TRO‐induced increase of survival. © 2002 Wiley‐Liss, Inc.