Caspase inhibition switches XXXX -induced apoptosis to senescence.

@entity632 @entity137 @entity522 @entity39 @entity5 @entity1194 @entity43190 @entity204 @entity994
The inhibition of apoptosis is generally believed to be a major determinant of resistance to chemotherapy. However, recent findings have shown that caspase inhibitors do not protect @entity5 cells from @entity204 by cytotoxic agents, but may switch drug-induced apoptosis to an alternative ' @entity204 '. The primary goals of this study were to determine the major characteristics of the ' @entity204 ' and the mechanism by which this switch is activated. For this purpose, we first investigated putative cell @entity204 modes induced by @entity632 . Molecular markers associated with these @entity204 modes were utilized to identify the @entity204 resulting from the inhibition of apoptosis. Our findings demonstrated that @entity632 induced at least three distinct types of cell @entity204 , senescence, apoptosis and a type of @entity39 , which were concentration dependent. Specific molecular markers such as @entity994 / @entity994 , activated @entity522 and activated Akt were associated with these @entity204 modes. The pan-caspase inhibitor ( @entity43190 ) greatly reduced @entity632 -induced @entity522 activation but did not protect cells against @entity137 . The combination of @entity632 and @entity43190 caused an increased expression of @entity994 / @entity994 and senescence -associated - @entity1194 activity, but did not alter Akt activation. Collectively, these findings suggest that the inhibition of apoptosis may lead to an increased expression of cell cycle inhibitors and cellular senescence.
