N-benzyl-5-phenyl-1H-pyrazole-3-carboxamide promotes vascular endothelial cell angiogenesis and migration in the absence of serum and FGF-2

Zhang, Haiyan; Su, Le; Huang, Bin; Zhao, Jing; Zhao, Bao‐Xiang; Zhang, Shangli; Jiang, Miao

doi:10.1038/aps.2010.201

Cited by 6 publications

(4 citation statements)

References 31 publications

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“…Our results are in agreement with the literature (Xiong et al, 2019) that reported a novel thiazolyl substituted bis-pyrazole oxime compound selectively inhibited proliferation of colorectal cancer HCT116 cells by inducing apoptosis pathway through the promotion of intracellular ROS level. The therapeutic impact of a Pyrazole compound on angiogenesis in human umbilical vein endothelial cells (HUVECs) was studied by Zhang et al, (2011). They showed the Pyrazole compound induced angiogenesis by a significant increase of NO and ROS production through ROS-HIF-1α-VEGF and NO signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Pyrazole Derivatives Induce Apoptosis via ROS Generation in the Triple Negative Breast Cancer Cells, MDA-MB-468

Ashourpour

Hosseini

Amini

et al. 2021

Asian Pac J Cancer Prev

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Breast cancer is one of the most common cancers among women and is a major reason for cancer death worldwide (Rakha et al., 2010). According to the literature, the incidence of female breast cancer in various countries was accounted for up to 3.2 million new cases per year by 2050 (Tao et al., 2015). Basically, breast cancer is a heterogeneous complex of diseases which involve a broad spectrum of subtypes (Yersal and Barutca, 2014).

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Section: Discussionmentioning

confidence: 99%

Pyrazole Derivatives Induce Apoptosis via ROS Generation in the Triple Negative Breast Cancer Cells, MDA-MB-468

Ashourpour

Hosseini

Amini

et al. 2021

Asian Pac J Cancer Prev

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“…The DCF assay is a popular method for assessing toxicant-stimulated generation of reactive oxidant species in cells (Bussche & Soares, 2011; Filipič & Hei, 2004; Gong & Han, 2006; Hatcher, et al, 2008; Hu, et al, 2011; Michalowicz, 2010; Naqvi, et al, 2010; Shanker & Aschner, 2003; Shao, et al, 2008; Wan & Winn, 2007; Zhang, et al, 2011; Zhu, et al, 2009). Although numerous caveats have been reported with the DCF assay, including effects of medium composition, serum, heme, heme proteins, metalloporphyrins and bovine serum albumin (Chen, et al, 2010), interactions with chemical toxicants have received nominal attention.…”

Section: Discussionmentioning

confidence: 99%

Troubleshooting the dichlorofluorescein assay to avoid artifacts in measurement of toxicant-stimulated cellular production of reactive oxidant species

Tetz

Kamau

Cheng

et al. 2013

Journal of Pharmacological and Toxicological Methods

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Introduction The dichlorofluorescein (DCF) assay is a popular method for measuring cellular reactive oxidant species (ROS). Although caveats have been reported with the DCF assay and other compounds, the potential for artifactual results due to cell-free interactions between the DCF compound and toxicants has hardly been explored. We evaluated the utility of the DCF assay for measuring ROS generation by the toxicants mono-(2-ethylhexyl) phthalate (MEHP), and tetrabromobisphenol A (TBBPA). Methods DCF fluorescence was measured spectrofluorometrically after a 1-h incubation of toxicants with 6-carboxy-2′,7′-dichlorodihydrofluorescein diacetate (carboxy-H2DCFDA). MEHP was incubated with carboxy-H2DCFDA in cell-free solutions of Hank’s buffered salt solution (HBSS), or in Royal Park Memorial Institute (RPMI) medium with or without fetal bovine serum. TBBPA was incubated with carboxy-H2DCFDA in cell-free HBSS and with human trophoblast cells (HTR8/SVneo cells). Results MEHP did not increase fluorescence in solutions of carboxy-H2DCFDA in HBSS or RPMI medium without serum. However, MEHP (90 and 180 μM) increased DCF fluorescence in cell-free RPMI medium containing serum. Furthermore, serum-free and cell-free HBSS solutions containing 25 μM TBBPA exhibited concentration-dependent increased fluorescence with 5–100 μM carboxy-H2DCFDA (p<0.05), but not 1 μM carboxy-H2DCFDA. In addition, we observed increased fluorescence in HTR8/SVneo cell cultures exposed to TBBPA (0.5–25 μM) (p<0.05), as we had observed in cell-free buffer. Discussion MEHP demonstrated an interaction with serum in cell-free generation of DCF fluorescence, whereas TBBPA facilitated conversion of carboxy-H2DCFDA to the fluorescent DCF moiety in the absence of serum. Because TBBPA increased fluorescence in the absence of cells, the increased DCF fluorescence observed with TBBPA in the presence of cells cannot be attributed to cellular ROS and may, instead, be the result of chemical activation of carboxy-H2DCFDA to the fluorescent DCF moiety. These data illustrate the importance of including cell-free controls when using the DCF assay to study toxicant-stimulated cellular production of ROS.

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“…To test the secreted VEGF, the medium was replaced with 1 ml per well of fresh medium, and the cells were subjected to normoxia or hypoxia in the absence or presence of PAB for 12 h. Then, the cell supernatants were collected for ELISA assays with a VEGF-ELISA kit (Jingmei, Shanghai, China) as previously described [17].…”

Section: Elisa Assaysmentioning

confidence: 99%

Pseudolaric acid B-driven phosphorylation of c-Jun impairs its role in stabilizing HIF-1alpha: a novel function-converter model

Wang

et al. 2012

J Mol Med

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We have recently discovered that c-Jun executes a non-transcriptional function to stabilize hypoxia inducible factor 1α (HIF-1α) and that pseudolaric acid B (PAB) accelerates HIF-1α degradation and phosphorylates c-Jun at Ser63/73. In this study, PAB was used as a probe to investigate whether and how the Ser63/73 phosphorylation of c-Jun regulates its functions. The PAB-induced reduction of HIF-1α protein was rescued through supplying additional non-phosphorylated c-Jun. However, c-Jun siRNA, which reduced both the PAB-driven phosphorylated c-Jun and the total c-Jun protein, did not prevent the PAB-induced decrease in HIF-1α. HIF-1α was revealed to be co-immunoprecipitated only with the non-phosphorylated c-Jun. PAB increased the phosphorylated c-Jun while reducing the non-phosphorylated c-Jun at Ser63/73, which impaired its function in stabilizing HIF-1α. Consequently, PAB led to the degradation of HIF-1α, thus resulting in the decreased HIF-1α-dependent expression of mdr-1 and VEGF. We accordingly propose a function-converter model of c-Jun: the Ser63/73 phosphorylation serves as a function converter to convert c-Jun from its non-transcriptional function to its transcriptional function.

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N-benzyl-5-phenyl-1H-pyrazole-3-carboxamide promotes vascular endothelial cell angiogenesis and migration in the absence of serum and FGF-2

Cited by 6 publications

References 31 publications

Pyrazole Derivatives Induce Apoptosis via ROS Generation in the Triple Negative Breast Cancer Cells, MDA-MB-468

Pyrazole Derivatives Induce Apoptosis via ROS Generation in the Triple Negative Breast Cancer Cells, MDA-MB-468

Troubleshooting the dichlorofluorescein assay to avoid artifacts in measurement of toxicant-stimulated cellular production of reactive oxidant species

Pseudolaric acid B-driven phosphorylation of c-Jun impairs its role in stabilizing HIF-1alpha: a novel function-converter model

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