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논문분류	춘계학술대회 초록집
제목	Endoplasmic Reticulum (ER) Stress Induces Epithelial-mesenchymal Transition (EMT) Through Induction of Autophagy in Tubular Epithelial Cells
저자	Soo Young Moon, Hyo Sang Kim, Kyeong Woo Nho, Young Joo Jang, Joon Seok Kim, Chung Hee Baek, Mi Yeon Kim, Sang Koo Lee
출판정보	2013; 2013(1):
키워드	Autophagy, EMT, ER stress
초록	Endoplasmic reticulum (ER) stress has been implicated in promoting epithelial-mesenchymal transition (EMT). ER stress is also known to induce autophagy. However, relationship between ER stress-induced autophagy and ER stress-induced EMT has not been explored so far. We hypothesized that ER stress might induce EMT through induction of autophagy in tubular epithelial cells. All experiments were performed using HK-2 cells. Protein expression was measured by Western blot analysis. Small interfering RNA (siRNA) experiment were also performed. Chemical ER stress inducer such as thapsigargin (TG, 0.2 uM) and tunicamycin (TM, 0.2 uM) induced autophagy, as shown by up-regulation of LC3-II and beclin. ER stress inhibitors such as 4-PBA and salubrinal suppressed the TGand TM-induced autophagy. TG and TM also induced EMT, as evidenced by conversion to fibroblast-like morphology, down-regulation of Ecadherin and up-regulation of α-smooth muscle actin, which were abolished by pretreatment with ER stress inhibitors. Transfection with siRNA targeting ER stress protein (IRE-1) also blocked the TG- and TM-induced autophagy and EMT. Suppression of TG- and TM- induced autophagy by autophagy inhibitors such as 3-methyladenine and bafilomycin inhibited the TG- and TM-induced EMT. siRNA targeting autophagy protein (beclin) also blocked the TG- and TMinduced EMT. As expected, an autophagy inducer, rapamycin, induced EMT as well. Both TG and TM activated the c-Src kinase and inhibitor of c-Src kinase (PP2) blocked the TG- or TM-induced autophagy and EMT. In conclusion, ER stress induced EMT through induction of autophagy in tubular epithelial cells, via c-Src kinase dependent pathway.
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