Elevated XXXX Signaling-Mediated Upregulation of MMP-2/9 Confers Enhanced Invasion Ability in Multidrug-Resistant Breast Cancer Cells.

@entity1 @entity5379 @entity0 @entity5 @entity4104 @entity1259 @entity3
UNASSIGNED: The development of multidrug resistance greatly impedes effective @entity5 therapy. Recent advances in @entity5 research have demonstrated that acquisition of multidrug resistance by @entity5 cells is usually accompanied by enhanced cell invasiveness. Several lines of evidence indicated that cross activation of other signaling pathways during development of drug resistance may increase invasive potential of multidrug-resistant (MDR) @entity5 cells. However, the accurate mechanism of this process is largely undefined. In this study, to better understand the associated molecular pathways responsible for @entity5 progression induced by drug resistance, a MDR @entity1 @entity0 cell line SK-BR-3/EPR with P-glycoprotein overexpression was established using stepwise long-term exposure to increasing concentration of @entity1259 . The SK-BR-3/EPR cell line exhibited decreased cell proliferative activity, but enhanced cell invasive capacity. We showed that the expression of metastasis-related @entity5379 was elevated in SK-BR-3/EPR cells. Moreover, SK-BR-3/EPR cells showed elevated activation of @entity4104 . Activation of @entity4104 signaling is responsible for enhanced invasiveness of SK-BR-3/EPR cells through upregulation of @entity5379 . @entity4104 is a well-known oncogene and is frequently implicated in tumorigenesis and chemotherapeutic resistance. Our findings augment insight into the mechanism underlying the functional association between MDR and @entity3 .
