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. 2019 Jun 18;18(2):1107–1114. doi: 10.3892/etm.2019.7681

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Copyright: © Song et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — TIM induced apoptosis through the NOXA/MCL-1 axis and triggering ER stress. U2OS cells were treated with 4 nM TIM for 48 h. (A) TIM treatment decreased the protein expression of MCL-1, but increased the protein expression of NOXA. (B) PGE1 (100 nM) inhibited the anti-proliferative effects of TIM. (C) Gene and (D) protein expression levels of the ER stress-marker proteins IRE1, ATF6 and GRP78 were increased by TIM. Data are expressed as the mean ± standard deviation (n=3). *P<0.05 and **P<0.01, vs. control group; ^##P<0.01, vs. TIM alone. TIM, (3R)-5,6,7-trihydroxy-3-isopropyl-3-methylisochroman-1-one; ER, endoplasmic reticulum; GRP78, glucose-regulated protein 78; IRE1, inositol-requiring enzyme 1; ATF6, activating transcription factor 6; PGE1, prostaglandin E1.