@entity7242 / @entity4104 -dependent heme oxygenase-1 induction mediates chemoresistance of @entity0 cells to XXXX by promoting autophagy.

@entity632 @entity1 @entity137 @entity7242 @entity0 @entity5 @entity4104 @entity13975 @entity3105 @entity204
Chemotherapeutic resistance in @entity0 , whether acquired or intrinsic, remains a major clinical obstacle. Thus, increasing @entity5 cell sensitivity to chemotherapeutic agents will be helpful in improving the clinical management of @entity0 . In the present study, we found an induction of @entity13975 expression in @entity632 ( @entity3105 )-treated MDA-MB-231 @entity1 @entity0 cells, which showed insensitivity to @entity3105 treatment. Knockdown @entity13975 expression dramatically upregulated the incidence of MDA-MB-231 cell @entity204 under @entity3105 treatment, indicating that @entity13975 functions as a critical contributor to drug resistance in MDA-MB-231 cells. We further observed that @entity3105 exposure induced a cytoprotective autophagic flux in MDA-MB-231 cells, which was dependent on @entity13975 induction. Moreover, upregulation of @entity13975 expression required the activation of both @entity4104 and its upstream regulator, protein kinase @entity7242 . Abrogating @entity7242 / @entity4104 pathway activation attenuated @entity13975 and autophagy induction, thus increasing the chemosensitivity of MDA-MB-231 cells. Therefore, we conclude that @entity7242 / @entity4104 -dependent @entity13975 induction protects MDA-MB-231 @entity0 cells from @entity3105 -induced @entity204 through promoting autophagy. In the following study, we further demonstrated the contribution of @entity7242 / @entity4104 / @entity13975 /autophagy pathway activation to @entity3105 resistance in another @entity0 cell line, MDA-MB-468, which bears a similar phenotype to MDA-MB-231 cells. Therefore, activation of @entity7242 / @entity4104 / @entity13975 /autophagy signaling pathway might play a general role in protecting certain subtypes of @entity0 cells from @entity3105 -induced @entity137 . Targeting this signaling event may provide a potential approach for overcoming @entity3105 resistance in @entity0 therapeutics.
