TGF-β Decreases the Stability of IL-18-Induced IFN-γ mRNA through the Expression of TGF-β-Induced Tristetraprolin in KG-1 Cells

Inoue, Yasumichi; Abe, Kenji; Onozaki, Kikuo; Hayashi, Hidetoshi

doi:10.1248/bpb.b14-00673

Cited by 11 publications

(10 citation statements)

References 51 publications

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“…Total RNA extraction was performed as previously described [ 38 ]. First-strand cDNA was synthesized with the PrimeScript first-strand cDNA Synthesis Kit (TaKaRa Bio Inc., Shiga, Japan) as previously described [ 35 ].…”

Section: Methodsmentioning

confidence: 99%

Anti-Tumorigenic Activity of Chrysin from Oroxylum indicum via Non-Genotoxic p53 Activation through the ATM-Chk2 Pathway

et al. 2018

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The p53 tumor suppressor plays critical roles in cell cycle regulation and apoptotic cell death in response to various cellular stresses, thereby preventing cancer development. Therefore, the activation of p53 through small molecules is an attractive therapeutic strategy for the treatment of cancers retaining wild-type p53. We used a library of 700 Myanmar wild plant extracts to identify small molecules that induce p53 transcriptional activity. A cell-based screening method with a p53-responsive luciferase-reporter assay system revealed that an ethanol extract of Oroxylum indicum bark increased p53 transcriptional activity. Chrysin was isolated and identified as the active ingredient in the O. indicum bark extract. A treatment with chrysin increased p53 protein expression and the p53-mediated expression of downstream target genes, and decreased cell viability in MCF7 cells, but not in p53-knockdown MCF7 cells. We also found that chrysin activated the ATM-Chk2 pathway in the absence of DNA damage. Hence, the inactivation of the ATM-Chk2 pathway suppressed p53 activation induced by chrysin. These results suggest the potential of chrysin as an anti-cancer drug through the activation of p53 without DNA damage.

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Section: Methodsmentioning

confidence: 99%

Anti-Tumorigenic Activity of Chrysin from Oroxylum indicum via Non-Genotoxic p53 Activation through the ATM-Chk2 Pathway

et al. 2018

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“…Total RNA extractions were performed as previously described 61 . First-strand cDNA was synthesized with PrimeScript first-strand cDNA Synthesis Kit (TaKaRa Bio Inc.) as previously described 60 .…”

Section: Methodsmentioning

confidence: 99%

“…PCR was performed using AmpliTaq Gold 360 Mater Mix (Applied Biosystems) and a 2720 Thermal Cycler 2700 (Applied Biosystems). The following primer sequences were used: human p53 , 5′-CTCACCATCATCACACTGGAAGAC-3′ (forward) and 5′-AGAGGAGCTGGTGTTGTTGGGCAG-3′ (reverse); human GAPDH , 5′-TGAAGGTCGGAGTCAACGGATTTGGT-3′ (forward) and 5′-CATGTGGGCCATGAGGTCCACCAC-3′ (reverse) 61 ; human PAI-1 , 5′-CATGGGGCCATGGAACAAGG-3′ (forward) and 5′-CTTCCTGAGGTCGACTTCAG-3′ (reverse); human TTP , 5′-TCATCCACAACCCTAGCGAA-3′ (forward) and 5′-GATGCGATTGAAGATGGGGA-3′ (reverse) 61 ; human p63 , 5′-CCAGACTCAATTTAGTGAGC-3′ (forward) and 5′-ACTTGCCAGATCATCCATGG-3′ (reverse) 57 ; mouse p53 , 5′-GATGACTGCCATGGAGGAGT-3′ (forward) and 5′-CTCGGGTGGCTCATAAGGTA-3′ (reverse) 62 ; mouse GAPDH , 5′-GGCATTGTGGAAGGGCTCA-3′ (forward) and 5′-TCCACCACCCTGTTGCTGT-3′ (reverse) 63 ; mouse PAI-1 , 5′-GGGAAAAGGGGCTGTGTGAC-3′ (forward) and 5′-GTACACGGTGTGTGGCTGTC-3′ (reverse) 64 ; and mouse p21 , 5′-TGTCTTGCACTCTGGTGTCTGAGC-3′ (forward) and 5′-TCTTGCAGAAGACCAATCTGCG-3′ (reverse) 65 . PCR amplification was performed in the linear range and PCR products were separated by 1.5–2% agarose gel electrophoresis 55 .…”

Section: Methodsmentioning

confidence: 99%

TGF-β induces p53/Smads complex formation in the PAI-1 promoter to activate transcription

Kawarada

Inoue

Kawasaki

et al. 2016

Sci Rep

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Transforming growth factor β (TGF-β) signaling facilitates tumor development during the advanced stages of tumorigenesis, but induces cell-cycle arrest for tumor suppression during the early stages. However, the mechanism of functional switching of TGF-β is still unknown, and it is unclear whether inhibition of TGF-β signaling results amelioration or exacerbation of cancers. Here we show that the tumor suppressor p53 cooperates with Smad proteins, which are TGF-β signal transducers, to selectively activate plasminogen activator inhibitor type-1 (PAI-1) transcription. p53 forms a complex with Smad2/3 in the PAI-1 promoter to recruit histone acetyltransferase CREB-binding protein (CBP) and enhance histone H3 acetylation, resulting in transcriptional activation of the PAI-1 gene. Importantly, p53 is required for TGF-β-induced cytostasis and PAI-1 is involved in the cytostatic activity of TGF-β in several cell lines. Our results suggest that p53 enhances TGF-β-induced cytostatic effects by activating PAI-1 transcription, and the functional switching of TGF-β is partially caused by p53 mutation or p53 inactivation during cancer progression. It is expected that these findings will contribute to optimization of TGF-β-targeting therapies for cancer.

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“…Luciferase activity was normalized to β-gal activity. 20) RNA Extraction, Reverse Transcription, and Quantitative PCR (qPCR) Total RNA was extracted as described previously. 21) First-strand cDNAs were synthesized with the PrimeScript first-strand cDNA synthesis kit (TaKaRa Bio Inc., Shiga, Japan) as previously described.…”

Section: Methodsmentioning

confidence: 99%

Lysine-Specific Demethylase 1 (LSD1/KDM1A) Is a Novel Target Gene of c-Myc

Nagasaka

Tsuzuki

Ozeki

et al. 2019

Biological & Pharmaceutical Bulletin

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Lysine-specific demethylase 1 (LSD1/KDM1A) is a histone demethylase and specifically catalyzes the demethylation of mono-and di-methylated histone H3 lysine 4 (H3K4). The LSD1-mediated demethylation of H3K4 promotes the assembly of the c-Myc-induced transcription initiation complex. Although LSD1 and c-Myc are both strongly expressed in human cancers, the mechanisms by which their activities are coordinated remain unclear. We herein demonstrated that LSD1 is a direct target gene of c-Myc. The knockdown of c-Myc decreased the expression of LSD1 in several cancer cell lines. We identified two non-canonical Eboxes in the proximal promoter region of the LSD1 gene. A chromatin immunoprecipitation assay showed that c-Myc bound to these E-boxes in the LSD1 promoter. Importantly, LSD1 mRNA expression correlated with c-Myc expression in human acute myeloid leukemia (AML), glioblastoma, stomach adenocarcinoma, and prostate adenocarcinoma. The present results suggest that LSD1 is induced by c-Myc and forms a positive feedback mechanism in transcription reactions by c-Myc.

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TGF-β Decreases the Stability of IL-18-Induced IFN-γ mRNA through the Expression of TGF-β-Induced Tristetraprolin in KG-1 Cells

Cited by 11 publications

References 51 publications

Anti-Tumorigenic Activity of Chrysin from Oroxylum indicum via Non-Genotoxic p53 Activation through the ATM-Chk2 Pathway

Anti-Tumorigenic Activity of Chrysin from Oroxylum indicum via Non-Genotoxic p53 Activation through the ATM-Chk2 Pathway

TGF-β induces p53/Smads complex formation in the PAI-1 promoter to activate transcription

Lysine-Specific Demethylase 1 (LSD1/KDM1A) Is a Novel Target Gene of c-Myc

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