XXXX homeostasis in @entity694 LoVo cells sensitive or resistant to @entity632 .

@entity632 @entity31566 @entity46404 @entity5 @entity46756 @entity694 @entity1760
UNASSIGNED: Neoplastic cells accumulate @entity1760 , an event which provides selective advantages and is frequently associated with @entity46756 overexpression. Little is known about @entity1760 homeostasis in @entity5 cells. Therefore, we used the @entity694 LoVo cell model and compared @entity632 -resistant to sensitive cells. In resistant cells the concentration of total @entity1760 is higher while its influx capacity is lower than in sensitive cells. Accordingly, resistant cells express lower amounts of the @entity31566 and 7, both involved in @entity1760 transport. While decreased @entity31566 levels are due to transcriptional regulation, post-transcriptional events are involved in reducing the amounts of @entity46756 . Indeed, the calpain inhibitor @entity46404 markedly increases the levels of @entity46756 in resistant cells. In @entity632 -sensitive cells, silencing @entity46756 shifts the phenotype to one more similar to resistant cells, since in these cells silencing @entity46756 significantly decreases the influx of @entity1760 , increases its intracellular concentration and increases resistance to @entity632 . On the other hand, calpain inhibition upregulates @entity46756 , decreases intracellular @entity1760 and enhances the sensitivity to @entity632 of resistant LoVo cells. We conclude that in LoVo cells drug resistance is associated with alteration of @entity1760 homeostasis through modulation of @entity46756 . Our data suggest that @entity46756 expression may be an additional undisclosed player in chemoresistance.
