scholarly journals Engineering caspase 7 as an affinity reagent to capture proteolytic products

FEBS Journal ◽  
2020 ◽  
Author(s):  
Amir S. Razai ◽  
Scott J. Snipas ◽  
Marcin Poreba ◽  
Domenico Fasci ◽  
Guy S. Salvesen
Keyword(s):  
Caspase 7 ◽  
Affinity Reagent

Proteasome inhibitor MG132 induces apoptosis in human osteosarcoma U2OS cells

2021 ◽  
pp. 096032712110179
Author(s):  
Han Ki Lee ◽  
See-Hyoung Park ◽  
Myeong Jin Nam
Keyword(s):  
Signaling Pathways ◽  
Proteasome Inhibitor ◽  
Migration And Invasion ◽  
Apoptotic Signaling ◽  
Antiapoptotic Proteins ◽  
Human Osteosarcoma ◽  
Anticancer Effects ◽  
Caspase 7 ◽  
U2os Cells ◽  
Western Blotting Assay

MG132 is a potent, reversible, and cell-permeable 20S proteasome inhibitor and it is derived from a Chinese medicinal plant. The purpose of this study is to investigate the anticancer effects of MG132 against human osteosarcoma U2OS cells. We first performed MTT and colony formation assays to investigate the anti-proliferative effects of MG132. The results demonstrated that MG132 suppressed the proliferation of U2OS cells. Furthermore, we found that treatment with MG132 increased apoptosis and induced DNA damage in U2OS cells. Additionally, zymography, wound healing, and invasion assays showed that MG132 suppressed the enzymatic activity of matrix metalloproteinases, cell migration, and invasion, respectively of U2OS cells. Furthermore, western blotting assay was performed to investigate the apoptotic signaling pathways in MG132-treated U2OS cells. Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells. These results demonstrated that MG132 activated apoptotic signaling pathways in U2OS cells. Interestingly, MG132 downregulated the phosphorylation of Akt and Erk. Taken together, our results suggest that MG132 has anticancer effects in U2OS cells. Therefore, MG132 may be a potential therapeutic agent for the treatment of osteosarcoma.

ChemInform Abstract: A Photolabile Disaccharide-C-glycoside as an Affinity Reagent for IgA X24.

ChemInform ◽  
1989 ◽  
Vol 20 (33) ◽  
Author(s):  
C.-S. KUHN ◽  
C. P. J. GLAUDEMANS ◽  
J. LEHMANN
Keyword(s):  
Affinity Reagent

Antiapoptotic function of Bcl-2 in mast cells is dependent on its association with heat shock protein 90β

Blood ◽  
2006 ◽  
Vol 107 (4) ◽  
pp. 1413-1420 ◽  
Author(s):  
Cellina Cohen-Saidon ◽  
Irit Carmi ◽  
Avishai Keren ◽  
Ehud Razin
Keyword(s):  
Mast Cell ◽  
Rna Interference ◽  
Mast Cells ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Caspase 3 ◽  
Caspase 7 ◽  
Antiapoptotic Activity ◽  
Novel Strategy ◽  
First Time

In the present study, we demonstrated that the antiapoptotic function of Bcl-2 in mast cells is significantly dependent on its association with the heat shock protein 90β (Hsp90β). Dissociation of these 2 proteins inhibits the antiapoptotic activity of Bcl-2 by initiating the release of cytochrome c from mitochondria into cytosol and increasing the activity of caspase 3 and caspase 7, resulting in mast-cell apoptosis. The antiapoptotic activity of Bcl-2 was greatly affected by knocking-out specifically Hsp90β using the RNA interference approach. Thus, for the first time, it has been shown that Hsp90β might modulate the antiapoptotic activity of Bcl-2 at least in mast cells. These findings could have implications for a novel strategy of regulating apoptosis in patients with mastocytosis and other mast cell–associated diseases.

scholarly journals Apoptosis Induction of Agave lechuguilla Torrey Extract on Human Lung Adenocarcinoma Cells (SK-LU-1)

2018 ◽  
Vol 19 (12) ◽  
pp. 3765 ◽  
Author(s):  
Luis Anguiano-Sevilla ◽  
Eugenia Lugo-Cervantes ◽  
Cynthia Ordaz-Pichardo ◽  
Jorge Rosas-Trigueros ◽  
María Jaramillo-Flores
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Ethanol Extract ◽  
Fragmentation Pattern ◽  
Intrinsic Pathway ◽  
Adenocarcinoma Cells ◽  
Human Lung Adenocarcinoma Cells ◽  
Caspase 7 ◽  
Mcf 7 ◽  
Apoptotic Signal

In this study, an ethanol extract of Agave lechuguilla was evaluated against six carcinogenic cell lines (HCT-15, MCF-7, PC-3, U-251, SK-LU-1 and K-562) with an inhibition of 75.7 ± 2.3% against the SK-LU-1 line. Based on the previous result, the extract was hydrolyzed and fractionated, to which the IC50 was determined; the cell line was more sensitive to the fractionated extract with an IC50 6.96 ± 0.15 µg/mL. Characterization by mass spectrometry showed the presence of kaempferol, quercetin and a flavonoid dimer formed by afzelechin-4β-8-quercetin, according to the generated fragmentation pattern. The fractionated extract presented cell death by apoptosis with 39.8% at 24 h. Molecular docking was performed with the molecules found to try to describe cell death by apoptosis through death receptors such as FasCD95, TNF-R1, DR4/5 and blocking signaling on the EGFR and K-Ras MAPK/ERK pathway, as well as through the intrinsic pathway activating tBID, which promotes the amplification of the apoptotic signal due to the activation of caspase-3, and consequently caspase-7. In addition to the activation of the IIb complex associated with cell death due to necroptosis.

scholarly journals Inactivating mutations of CASPASE-7 gene in human cancers

Oncogene ◽  
2003 ◽  
Vol 22 (39) ◽  
pp. 8048-8052 ◽  
Author(s):  
Young Hwa Soung ◽  
Jong Woo Lee ◽  
Hong Sug Kim ◽  
Won Sang Park ◽  
Su Young Kim ◽  
...  
Keyword(s):  
Human Cancers ◽  
Caspase 7 ◽  
Inactivating Mutations

scholarly journals MicroRNA-224 is implicated in lung cancer pathogenesis through targeting caspase-3 and caspase-7

Oncotarget ◽  
2015 ◽  
Vol 6 (26) ◽  
pp. 21802-21815 ◽  
Author(s):  
Ri Cui ◽  
Taewan Kim ◽  
Matteo Fassan ◽  
Wei Meng ◽  
Hui-Lung Sun ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Caspase 3 ◽  
Cancer Pathogenesis ◽  
Caspase 7

scholarly journals PECULIARITIES OF APOPTOTIC MARKER EXPRESSION IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND ARTERIAL HYPERTENSION

2018 ◽  
Vol 18 (4) ◽  
pp. 65-71
Author(s):  
O.S. Tyaglaya
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Essential Hypertension ◽  
Arterial Hypertension ◽  
Pulmonary Disease ◽  
Cysteine Proteases ◽  
Chronic Obstructive ◽  
Significant Elevation ◽  
Caspase 9 ◽  
Obstructive Pulmonary Disease ◽  
Caspase 7

It is known that both chronic obstructive pulmonary disease and arterial hypertension are multifactorial diseases, and develop as a result of a complex interaction of genetic and environmental factors. The purpose of this work was to study the metabolism of caspase-7 and caspase-9 in patients with chronic obstructive pulmonary disease (COPD) in combination with arterial hypertension (AH). Materials and methods. We examined 23 patients with a diagnosis of essential hypertension stage II and COPD stage II without a clinically significant concomitant pathology. The plasma level of caspase-7 and caspase-9 was determined using the appropriate ELISA test systems (manufacturer – Bender Medsystems, Austria) at the Medical and Laboratory Training Centre of Zaporizhzhia State Medical University in accordance with the instructions attached to the kit. The analysis of the dynamics of the studied cysteine ​​proteases indicates a statistically significant elevation of these apoptosis markers in the conditions of hypertension and COPD. The value of caspase-7 in the cohort of patients with COPD + AH significantly exceeded similar figures for the groups of patients with a single pathology presented by AH or COPD, and averaged 0.41 ± 0.09 ng / ml. A statistically significant elevation of the caspase-9 level in patients with COPD + AH up to 2.16 ± 0.29 ng / ml compared with other groups also indicates a more significant induction of apoptotic processes in comorbid pathology than in isolated AH or COPD. Conclusion. The obtained results require further clarification of the nature of the relationship between changes in the metabolism of cysteine ​​proteases and the primacy of pathogenetic processes in the mechanisms of risk formation for complications and progression of ventilation disorders in patients with COPD and comorbid essential hypertension.

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