YM155 sensitizes TRAIL-induced apoptosis through cathepsin S-dependent down-regulation of Mcl-1 and NF-κB-mediated down-regulation of c-FLIP expression in human renal carcinoma Caki cells

Woo, Seon Min; Min, Kyoung‐jin; Seo, Bo Ram; Kwon, Taeg Kyu

doi:10.18632/oncotarget.11137

Cited by 27 publications

(21 citation statements)

References 46 publications

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“…Our results also showed that the low, moderate and high doses of Junduqing extractive could reduce the expression of Mcl-1 and enhance the apoptosis of human NPC cells. This was consistent with the above reports [24][25][26]. These results suggested that the decrease of Mcl-1 expression might be responsible for the increase of human NPC cell apoptosis.…”

Section: Discussionsupporting

confidence: 93%

“…Rapid degradation of Mcl-1 may directly lead to cell apoptosis [25]. Downregulation of Mcl-1 expression induced by exogenous small-molecular inhibitor can trigger the apoptosis of human renal carcinoma (Caki) cells [26]. Our results also showed that the low, moderate and high doses of Junduqing extractive could reduce the expression of Mcl-1 and enhance the apoptosis of human NPC cells.…”

Section: Discussionmentioning

confidence: 54%

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Junduqing extractive promotes the apoptosis of nasopharyngeal carcinoma cells through down-regulating Mcl-1 and Bcl-xL and up-regulating Caspase-3, Caspase-8 and Caspase-9

Zhao

Tang

Gao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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This study aimed to investigate the effect of Junduqing extractive on proliferation, apoptosis, migration and invasion of nasopharyngeal carcinoma (NPC) cells and the involved mechanism. Junduqing extractive was prepared. CCK-8 assay found that IC50 of Junduqing extractive in HNE-1 cells was 2.99 mg/ml, so its concentration of 1.0, 2.0 and 3.0 mg/ml was selected to perform the following experiments. HNE-1, HNE-2 and HONE1 cells were then divided into four groups: (1) Control (no treatment); (2) 1.0 mg/ml (1.0 mg/ml Junduqing); (3) 2.0 mg/ml (2.0 mg/ml Junduqing) and (4) 3.0 mg/ml (3.0 mg/ml Junduqing). Cell viability, apoptosis, migration and invasion were examined by CCK-8 assay, annexin V-FITC/PI staining, scratch wound assay and transwell assay, respectively. Compared with the control group, the viability, migration rates and invasive capacity of HNE-1, HNE-2 and HONE1 cells with Junduqing treatments decreased significantly. Higher concentration of Junduqing extractive caused lower viability, smaller migration rates and weaker invasive capacity. Compared with the control group, the apoptosis of HNE-1, HNE-2 and HONE1 cells after treatment with 2.0 and 3.0 mg/ml of Junduqing extractive increased remarkably. Levels of Bcl-xL, Mcl-1, Caspase-3, Caspase-8 and Caspase-9 were examined by western blotting. Compared with the control group, the expression of Bcl-xL and Mcl-1 and the expression of Caspase-3, Caspase-8 and Caspase-9 in HNE-1, HNE-2 and HONE1 cells were significantly downregulated and up-regulated, respectively, after treatment with Junduqing extractive. In conclusion, Junduqing extractive could inhibit the proliferation, migration and invasion, and promote the apoptosis of human NPC cells through down-regulating Mcl-1 and Bcl-xL and up-regulating Caspase-3, Caspase-8 and Caspase-9.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 54%

Junduqing extractive promotes the apoptosis of nasopharyngeal carcinoma cells through down-regulating Mcl-1 and Bcl-xL and up-regulating Caspase-3, Caspase-8 and Caspase-9

Zhao

Tang

Gao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Previous studies reported that loss of mitochondria membrane potential (MMP) plays critical role in overcome of TRAIL resistance [ 31 , 32 ]. Therefore, we measured the loss of MMP using rhodamine123 fluorescence dye.…”

Section: Resultsmentioning

confidence: 99%

Up-regulation of 5-lipoxygenase by inhibition of cathepsin G enhances TRAIL-induced apoptosis through down-regulation of survivin

et al. 2017

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Cathepsin G is a serine protease secreted from activated neutrophils, it has important roles in inflammation and immune response. Moreover, cathepsin G promotes tumor cell-cell adhesion and migration in cancer cells. In this study, we investigated whether inhibition of cathepsin G could sensitize TRAIL-mediated apoptosis in cancer cells. An inhibitor of cathepsin G [Cathepsin G inhibitor I (Cat GI); CAS 429676-93-7] markedly induced TRAIL-mediated apoptosis in human renal carcinoma (Caki, ACHN, and A498), lung cancer (A549) and cervical cancer (Hela) cells. In contrast, combined treatment with Cat GI and TRAIL had no effect on apoptosis in normal cells [mesangial cell (MC) and human skin fibroblast (HSF)]. Cat GI induced down-regulation of survivin expression at the post-translational level, and overexpression of survivin markedly blocked apoptosis induced by combined treatment with Cat GI plus TRAIL. Interestingly, Cat GI induced down-regulation of survivin via 5-lipoxygenase (5-LOX)-mediated reactive oxygen species (ROS) production. Inhibition of 5-LOX by gene silencing (siRNA) or a pharmacological inhibitor of 5-LOX (zileuton) markedly attenuated combined treatment-induced apoptosis. Taken together, our results indicate that inhibition of cathepsin G sensitizes TRAIL-induced apoptosis through 5-LOX-mediated down-regulation of survivin expression.

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“…TRAIL inhibits Mcl-1 expression via activating the pro-apoptotic activity of p38 in the receptor interacting serine/threonine kinase 1-dependent pathway in H460 cells (27). It has also been demonstrated that YM155 sensitizes TRAIL-induced apoptosis via cathepsin S-dependent downregulation of Mcl-1 expression, and nuclear factor-κB-mediated downregulation of c-FLIP expression in Caki cells (28). In the present study, the expression of c-FLIP and Mcl-1 was higher in H460-TR cells compared with H460 cells.…”

Section: Discussionmentioning

confidence: 98%

β-catenin decreases acquired TRAIL resistance in non-small-cell lung cancer cells by regulating the redistribution of death receptors

et al. 2018

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Tumor necrosis factor‑related apoptosis‑inducing ligand (TRAIL) exhibits antitumor activity in various types of tumor cell and tumor‑bearing animals. However, acquired TRAIL resistance is a common issue that restricts its clinical application. Previous studies have revealed that β‑catenin is associated with TRAIL resistance in melanoma and colorectal tumors. In the present study, an acquired‑resistance non‑small‑cell lung cancer (NSCLC) cell line (H460‑TR) was established from parental TRAIL‑sensitive H460 cells using a gradient ascent model (8‑256 ng/ml TRAIL). Cellular FADD‑like interleukin‑1β converting enzyme inhibitory protein and Mcl‑1 were upregulated and the cell surface distribution of death receptor (DR)4 and DR5 was downregulated in H460‑TR cells compared with the parental H460 cells. The results of reverse transcription‑quantitative polymerase chain reaction and western blot analysis indicated that H460 cells expressed increased levels of β‑catenin and were more sensitive to TRAIL compared with H460‑TR cells. β‑catenin‑knockdown in H460 cells decreased their sensitivity to TRAIL, while upregulation of β‑catenin expression in H460‑TR cells increased their sensitivity to TRAIL, increased the cell surface distribution of DRs and activated caspase‑3/8. Taken together, the results of the present study suggest that β‑catenin impairs acquired TRAIL resistance in NSCLC cells by promoting the redistribution of DR4 and DR5 to the cytomembrane, and inducing TRAIL‑mediated cell apoptosis via caspase‑3/8 activation.

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YM155 sensitizes TRAIL-induced apoptosis through cathepsin S-dependent down-regulation of Mcl-1 and NF-κB-mediated down-regulation of c-FLIP expression in human renal carcinoma Caki cells

Cited by 27 publications

References 46 publications

Junduqing extractive promotes the apoptosis of nasopharyngeal carcinoma cells through down-regulating Mcl-1 and Bcl-xL and up-regulating Caspase-3, Caspase-8 and Caspase-9

Junduqing extractive promotes the apoptosis of nasopharyngeal carcinoma cells through down-regulating Mcl-1 and Bcl-xL and up-regulating Caspase-3, Caspase-8 and Caspase-9

Up-regulation of 5-lipoxygenase by inhibition of cathepsin G enhances TRAIL-induced apoptosis through down-regulation of survivin

β-catenin decreases acquired TRAIL resistance in non-small-cell lung cancer cells by regulating the redistribution of death receptors

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