XBP1S protects cells from ER stress-induced apoptosis through Erk1/2 signaling pathway involving CHOP

摘要: The mammalian unfolded protein response (UPR) protects the cell against stress of misfolded proteins in endoplasmic reticulum (ER), and transcription factor X-box binding 1 spliced (XBP1S), a regulator UPR, is known to be important for ER (ERS)-mediated apoptosis growth, but molecular mechanism underlying these processes remains unexplored. Here, we report that knockdown XBP1S by an siRNA silencing approach increased expression ERS-associated molecules. overexpression stimulated, whereas its inhibited, proliferation chondrocytes chondrosarcoma cells; addition, while repression enhanced, ERS-mediated cells. Furthermore, XBP1S-mediated inhibition ERS through Erk1/2 signaling pathway down-regulation CHOP factor. one key downstream molecules involved apoptosis. Collectively, findings reveal novel critical role mechanisms involved.