Overexpression of microRNA-182 (miR-182) is found in multiple cancers, but the 
association of miR-182 expression with the sensitivity of triple-negative breast 
cancer (TNBC) cells to tumor necrosis factor-alpha (TNF-α) remains unknown. In 
this study, up-regulation of miR-182 was validated in TNBC patients and cell 
lines. Knockdown of miR-182 was observed to hinder the proliferation of BT-549 
cells. More importantly, knockdown of miR-182 significantly promoted the 
apoptosis induced by TNF-α treatment in BT-549. JC-1 staining and western blot 
assays revealed that the K63-linked ubiquitin chains on receptor-interacting 
protein 1 (RIP1) were removed and the outer mitochondrial membrane potential 
(MMP) and permeability was altered upon combination of TNF-α with anti-miR-182. 
We then demonstrated that knockdown of miR-182 up-regulated the expression of 
cylindromatosis (CYLD) deubiquitinase, which promoted the formation of 
death-inducing signaling complex (DISC) and subsequent caspase-8 activation in 
TNF-α-treated BT-549 cells. Collectively, the results of the present study 
improve our understanding of the role of miR-182 in TNBC, knockdown of which 
facilitates the degradation of ubiquitin chains on RIP1, leading to the 
caspase-8 activation and apoptosis in TNF-α-treated TNBC cells. This may be 
valuable for the development of cancer therapy.