A Novel Aziridine-based Bruton’s Tyrosine Kinase Inhibitor Induces Apoptosis Through Down-regulation of p65/RelA Phosphorylation on Serine 536 and ERK1/2 in Mantle Cell Lymphoma

Romanchikova, Nadezhda; Strods, Arnis; Strazdina, J.; Strumfs, Boriss; Trapencieris, Pēteris

doi:10.21873/anticanres.11204

Cited by 3 publications

(2 citation statements)

References 51 publications

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“…Specifically, we identified and validated two target genes of miR-155-5p, Rela and Traf3, both related to AP, through analysis with the TargetScan software, luciferase gene reporter assays and a series of transfection experiments. The NF-ĸB family of transcription factors contains five members, p50, p52, p65 (Rela), Relb and c-Rel [28,29]. The NF-κB family of transcription factors plays important roles in a wide range of biological processes such as inflammation, immune responses, cell proliferation, cell differentiation, cell survival and apoptosis [30,31].…”

Section: Discussionmentioning

confidence: 99%

miR-155-5p is Negatively Associated with Acute Pancreatitis and Inversely Regulates Pancreatic Acinar Cell Progression by Targeting Rela and Traf3

Liu¹,

Zou²,

Wang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Acute pancreatitis contributes to high mortality in pancreatitis patients, and miRNAs play a vital role in the development of acute pancreatitis (AP), however, its precise biological role remains largely elusive. Methods: To clarify the potential mechanisms of miRNAs in AP, we built mouse models of mild acute pancreatitis (MAP) and moderate/ severe acute pancreatitis (SAP). MiRNA microarray analysis and Real-time quantitative PCR (qRT-PCR) were used to analyze the expression of miRNA in MAP/SAP. TargetScan software, dual-luciferase gene reporter assays and Western blotting were used to assess the target genes of miR-155-5p in AP. Results: miR-155-5p was significantly decreased in MAP/SAP mice compared to controls. In pancreatic acinar AR42J cells transfected with miR-155-5p mimic, the expression of Rela and Traf3 notably decreased in both the caerulein- and TLC-S-induced groups compared with the negative control (NC); however, the expression of Rela and Traf3 notably increased after transfection with miR-155-5p inhibitor. Combined analysis using the TargetScan software and dual-luciferase gene reporter assays indicated that Rela and Traf3 were both targeted by miR-155-5p. Meanwhile, the expression of Ptgs2 also decreased after transfection of the AR42J cells with miR-155-5p mimic. The opposite results were found when miR-155-5p inhibitor was transfected into the AR42J cells. In addition, we treated caerulein- and TLC-S-induced AR42J cells with the Rela inhibitor helenalin and found that the expression of Rela, Traf3 and Ptgs2 decreased compared with the NC, while the expression of miR-155-5p did not show any significant difference. Furthermore, we found that miR-155-5p was significantly down-regulated in pancreatitis patients. Conclusion: miR-155-5p inversely regulated AP development through the Rela/Traf3/Ptgs2 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

miR-155-5p is Negatively Associated with Acute Pancreatitis and Inversely Regulates Pancreatic Acinar Cell Progression by Targeting Rela and Traf3

Liu¹,

Zou²,

Wang³

et al. 2018

Cell Physiol Biochem

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“…WST-8 cell proliferation assay. To evaluate WL cytotoxicity, WST-8 assays (Cayman Chemicals, Ann Arbor, MI, USA) were performed according to manufacturer's protocol, as it was already described (22). All data are given as the mean of three independent experiments±standard deviation (SD).…”

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confidence: 99%

Wedelolactone Targets EZH2-mediated Histone H3K27 Methylation in Mantle Cell Lymphoma

Romanchikova

Trapencieris

2019

Anticancer Res

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Background/Aim: Enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive complex 2 (PRC2), possesses histone N-methyltransferase (HMT) activity and plays an essential role in cancer initiation and development. The aim of the present study was to investigate the potential of Wedelolactone (WL) to inhibit the methylation activity of EZH2. Materials and Methods: The mantle cell lymphoma (MCL) cell line, Mino, was treated with WL, while untreated cells were used as control. HMT activity and EZH2 amount were measured in nuclear extracts from WL-treated and control Mino cells. Results: WL was found to target EZH2-mediated histone H3K27 methylation. Along with the inhibition of H3K27 methylation in vitro (IC50=0.3 μM), WL suppressed HMT activity in Mino cells with an IC50 value of 3.2 μM. We detected a reduced amount of EZH2 in Mino cells treated with WL, compared to untreated control cells. Conclusion: This is the first study to show that WL induces inhibition of H3K27 methylation via EZH2 modulation and decreases cell proliferation in MCL, in vitro. WL is proposed as a promising agent and a novel epigenetic approach in MCL investigation and treatment. Materials and MethodsCell lines and cell culture. The MCL (non-Hodgkin's B-cell lymphoma) cell line, Mino, was obtained from American Type Cell 4179

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Caracasine acid, an ent-3,4-seco-kaurene, promotes apoptosis and cell differentiation through NFkB signal pathway inhibition in leukemia cells.

Martínez

Mijares

Chávez

et al. 2019

European Journal of Pharmacology

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A Novel Aziridine-based Bruton’s Tyrosine Kinase Inhibitor Induces Apoptosis Through Down-regulation of p65/RelA Phosphorylation on Serine 536 and ERK1/2 in Mantle Cell Lymphoma

Cited by 3 publications

References 51 publications

miR-155-5p is Negatively Associated with Acute Pancreatitis and Inversely Regulates Pancreatic Acinar Cell Progression by Targeting Rela and Traf3

miR-155-5p is Negatively Associated with Acute Pancreatitis and Inversely Regulates Pancreatic Acinar Cell Progression by Targeting Rela and Traf3

Wedelolactone Targets EZH2-mediated Histone H3K27 Methylation in Mantle Cell Lymphoma

Caracasine acid, an ent-3,4-seco-kaurene, promotes apoptosis and cell differentiation through NFkB signal pathway inhibition in leukemia cells.

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