Inhibition of @entity2284 and @entity6641 potentiates @entity1487 and XXXX mediated cell killing in @entity157 cells.

@entity522 @entity2284 @entity1457 @entity3003 @entity6641 @entity157 @entity3092 @entity1487
@entity1457 ( @entity1457 ) modulate several cellular functions and are ubiquitously present in cell. Here, we investigated alterations in the expression of @entity1457 and explored functional consequences of the same. Moreover, effect of @entity3092 (Qctn), an inhibitor of @entity1457 , on chemotherapeutic drugs treatment in @entity157 cells Hep3B and HepG2 was investigated. We for the first time report that @entity1487 ( @entity1487 ) and @entity3003 specifically induce expression of @entity6641 in addition to @entity2284 in Hep3B and HepG2 cells. Induction of @entity1457 following exposure to sub lethal dose of drugs is a cellular challenge to survival. However, under lethal environmental conditions with reduced cell viability, cells fail to sustain the induction of survival proteins, @entity2284 and @entity6641 . Though Qctn itself, to certain extent is cytotoxic to cells, it potentiates the pro-apoptotic action of @entity1487 and @entity3003 , by inhibiting expression of @entity1457 . The increased cell killing correlates with decreased levels of @entity522 . Furthermore, siRNA mediated knockdown of @entity2284 and @entity6641 diminishes survival of drugs exposed cells. Altogether, our data provides clear evidence that @entity2284 and 40 promote cell survival and inhibition of their expression does not allow cells to adapt to drug exposure and survive. Collectively, our novel findings on compelling action of @entity1487 or @entity3003 following knockdown of @entity6641 and that of @entity2284 highlights their strategic implications towards an effective therapy against @entity157 .
