Alterations in the nucleocytoplasmic transport in apoptosis: Caspases lead the way

Kopeina, Gelina S.; Prokhorova, Evgeniia; Lavrik, Inna N.; Zhivotovsky, Boris

doi:10.1111/cpr.12467

Cited by 49 publications

(38 citation statements)

References 138 publications

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“…Caspase 3 and Caspase 9 are closely associated with apoptosis, and once apoptosis is initiated, the caspase cascade is initiated by apoptotic proteases, which induces irreversible apoptosis. Apoptosis is strictly regulated, and the normal cell caspases are in the non-activated zymogen state (29). In the present study, following treatment with propofol, the expression of the pro-apoptotic protein Bax, was increased, and as the concentration of propofol was increased, the apoptotic effect was enhanced accordingly.…”

Section: Discussionsupporting

confidence: 46%

Propofol induces ROS‑mediated intrinsic apoptosis and migration in triple‑negative breast cancer cells

Wang¹,

Zhao

et al. 2020

Oncol Lett

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Propofol is widely applied in general anesthesia owing to its short effect and rapid recovery. Apart from its anesthetic advantages, propofol has also been observed to inhibit the growth of several types of cancer cells. Breast cancer is the most diagnosed cancer in females worldwide and triple negative breast cancer (TNBC) constitutes 15-20% of all breast cancer cases. TNBC is characterized by a high recurrence rate, which is associated with its high mortality rate. The present study aimed to evaluate apoptosis in MDA-MB-468 cells treated with propofol. The Cell Counting Kit-8 assay was used to assess proliferation in cells treated with different concentrations of propofol. In addition, Annexin V-FITC was used to detect apoptosis. Furthermore, the generation of reactive oxygen species (ROS) was examined. The relative expression of proteins in the intrinsic apoptosis pathway, such as Bak, Bax, Bcl-2, Cytochrome c, apoptotic peptidase-activating factor 1 (Apaf-1), Caspase 3 and Caspase 9, were calculated relative to GAPDH with western blot analysis. A wound healing assay was performed to examine the effect of propofol on MDA-MB-468 cell migration. The present study revealed that propofol inhibited the proliferation and increased the level of ROS in MDA-MB-468 cells. The expression levels of Cytochrome c, Apaf-1, Bax, Bak and cleaved Caspase 3/9 were upregulated compared with GAPDH. The level of Bcl-2 protein was upregulated by propofol at a concentration of 5 µM and downregulated at concentrations of 10 and 20 µM. In the wound-healing assay, propofol reduced the scratch distance and area. Taken together, the results of the present study suggested that propofol may induce ROS-mediated intrinsic apoptosis and promote migration in TNBC cells.

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Section: Discussionsupporting

confidence: 46%

Propofol induces ROS‑mediated intrinsic apoptosis and migration in triple‑negative breast cancer cells

Wang¹,

Zhao

et al. 2020

Oncol Lett

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“…Thus, CHOP is considered as a marker of ER stress. Caspase could control the occurrence and progression of apoptosis by causing nuclear shrinkage and DNA segmentation to form apoptosis through cleaving protein kinases, nucleases and cytoskeleton [10,11]. Among them, caspase3 is the most important effector protease in the caspase cascade [12].…”

Section: Introductionmentioning

confidence: 99%

Ketamine induces endoplasmic reticulum stress in rats and SV-HUC-1 human uroepithelial cells by activating NLRP3/TXNIP aix

et al. 2019

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Many clinical studies have been conducted on ketamine-associated cystitis. However, the underlying mechanisms of ketamine-associated cystitis still remain unclear. Bladder tissues of rats were stained by Hematoxylin and Eosin (HE). The viability of human uroepithelial cells (SV-HUC-1 cells) was determined by cell counting kit-8 (CCK-8). Apoptosis and reactive oxygen species (ROS) were examined by flow cytometry. Additionally, the expressions of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1β and IL-18 were respectively determined by reverse transcription quantitative (RTq)-PCR and enzyme-linked immunosorbent assay (ELISA). The mRNA and protein levels of B-cell lymphoma/leukemia-2 (Bcl2), Bcl-2-associated X protein (Bax), cleaved caspase 3, glucose-regulated protein 78 (GRP78), CCAAT/enhancer binding protein homologous protein (CHOP), NOD-like receptor 3 (NLRP3), thioredoxin-interacting protein (TXNIP), Catalase and MnSOD were examined by RT-qPCR and Western blot. Small interfering RNA target TXNIP transfection was performed using Lipofectamine™ 2000. We found that ketamine effectively damaged bladder tissues of rats and promoted apoptosis through regulating the expression levels of GRP78, CHOP, Bcl-2, Bax and cleaved Caspase-3 proteins in vivo and in vitro. NLRP3 inflammatory body and TXNIP were activated by ketamine, which was supported by the changes in TNF-α, IL-6, IL-1 and IL-18 in vivo and in vitro. Furthermore, knocking down TXNIP reversed the effects of ketamine on apoptosis and NLRP3 inflammatory body in SV-HUC-1 cells. Meanwhile, the changes of Catalase and MnSOD showed that ROS was enhanced by ketamine, however, such an effect was ameliorated by down-regulation of TXNIP in SV-HUC-1 cells. Ketamine promoted cell apoptosis and induced inflammation in vivo and in vitro by regulating NLRP3/TXNIP aix.

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“…The mitochondrial pathway is characterized by mitochondrial membrane depolarization, which results in the release of cytochrome c, followed by caspase3 activation ( Yang et al, 2010 ). As a family of specific cysteine proteases and caspases can cleave substrates located in intracellular compartments that are initiators and executors of apoptosis, including caspase3, 6, 8, 9, and 10 ( Park et al, 2007 ; Kopeina et al, 2018 ). Among these, caspase3 has been known as the death protease because of the critical role it plays in cell apoptosis, which has been reported to be activated in ONFH ( Scarabelli et al, 2004 ; Yang et al, 2010 ; Abdi et al, 2011 ; Cui et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

The Protective Effect of Luteolin in Glucocorticoid-Induced Osteonecrosis of the Femoral Head

Yan

Zhan

et al. 2020

Front. Pharmacol.

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Glucocorticoid-induced osteonecrosis of the femoral head (GIONFH) is a frequently occurring type of nontraumatic osteonecrosis. A failure of the timely treatment can eventually result in the collapse of the subchondral bone structure. Luteolin (Lut), a compound extracted from Rhizoma Drynariae, is reported to possess multiple pharmacological properties including anticancer, antioxidant, antiapoptosis, and antiinflammatory properties. However, whether Lut has a protective effect on the development of GIONFH remains unclear. In this study, we evaluated the effect of Lut on Dexamethasone (Dex)-induced STAT1/caspase3 pathway in vitro and evaluated GIONFH model in vivo. In vitro, Lut inhibited the upregulation of Dex-induced phospho-STAT1, cleaved caspase9, and cleaved caspase3. In addition, Lut inhibited Dex-induced expression of Bax and cytochrome c and increased the expression of B cell lymphoma-2 (Bcl-2). In vivo, Lut decreased the proportion of empty lacunae in rats with GIONFH. Taken together, these findings indicate that Lut may have therapeutic potential in the treatment of GIONFH. Further, this effect might be achieved by suppressing mitochondrial apoptosis of osteoblasts via inhibition of STAT1 activity.

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Alterations in the nucleocytoplasmic transport in apoptosis: Caspases lead the way

Cited by 49 publications

References 138 publications

Propofol induces ROS‑mediated intrinsic apoptosis and migration in triple‑negative breast cancer cells

Propofol induces ROS‑mediated intrinsic apoptosis and migration in triple‑negative breast cancer cells

Ketamine induces endoplasmic reticulum stress in rats and SV-HUC-1 human uroepithelial cells by activating NLRP3/TXNIP aix

The Protective Effect of Luteolin in Glucocorticoid-Induced Osteonecrosis of the Femoral Head

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