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Article ; Online: Regulation of signal transducer and activator of transcription 3 activation by dual-specificity phosphatase 3.

Kim, Ba Reum / Ha, Jain / Kang, Eunjeong / Cho, Sayeon

2020 Volume 53, Issue 6, Page(s) 335–340

Abstract: Since cancer is the leading cause of death worldwide, there is an urgent need to understand the mechanisms underlying cancer progression and the development of cancer inhibitors. Signal transducer and activator of transcription 3 (STAT3) is a major ... ...

Abstract	Since cancer is the leading cause of death worldwide, there is an urgent need to understand the mechanisms underlying cancer progression and the development of cancer inhibitors. Signal transducer and activator of transcription 3 (STAT3) is a major transcription factor that regulates the proliferation and survival of various cancer cells. Here, dual-specificity phosphatase 3 (DUSP3) was identified as a regulator of STAT3 based on an interaction screening performed using the protein tyrosine phosphatase library. DUSP3 interacted with the C-terminal domain of STAT3 and dephosphorylated p-Y705 of STAT3. In vitro dephosphorylation assay revealed that DUSP3 directly dephosphorylated p-STAT3. The suppressive effects of DUSP3 on STAT3 were evaluated by a decreased STAT3-specific promoter activity, which in turn reduced the expression of the downstream target genes of STAT3. In summary, DUSP3 downregulated the transcriptional activity of STAT3 via dephosphorylation at Y705 and also suppressed the migratory activity of cancer cells. This study demonstrated that DUSP3 inhibits interleukin 6 (IL-6)/STAT3 signaling and is expected to regulate cancer development. Novel functions of DUSP3 discovered in IL-6/STAT3 signaling regulation would help expand the understanding of cancer development mechanisms. [BMB Reports 2020; 53(6): 335-340].
MeSH term(s)	Cells, Cultured ; Dual Specificity Phosphatase 3/metabolism ; Humans ; Interleukin-6/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction
Chemical Substances	Interleukin-6 ; STAT3 Transcription Factor ; STAT3 protein, human ; DUSP3 protein, human (EC 3.1.3.48) ; Dual Specificity Phosphatase 3 (EC 3.1.3.48)
Language	English
Publishing date	2020-05-30
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2410389-5
ISSN	1976-670X ; 1976-6696
ISSN (online)	1976-670X
ISSN	1976-6696
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Anti-inflammatory effects of a novel compound, MPQP, through the inhibition of IRAK1 signaling pathways in LPS-stimulated RAW 264.7 macrophages.

Kim, Ba Reum / Cho, Young-Chang / Cho, Sayeon

BMB reports

2018 Volume 51, Issue 6, Page(s) 308–313

Abstract: Small-molecule inhibitors are widely used to treat a variety of inflammatory diseases. In this study, we found a novel antiinflammatory compound, 1-[(2R,4S)-2-methyl-4-(phenylamino)-1,2,3,4-tetrahydroquinolin-1-yl]prop-2-en-1-one (MPQP). It showed strong ...

Abstract	Small-molecule inhibitors are widely used to treat a variety of inflammatory diseases. In this study, we found a novel antiinflammatory compound, 1-[(2R,4S)-2-methyl-4-(phenylamino)-1,2,3,4-tetrahydroquinolin-1-yl]prop-2-en-1-one (MPQP). It showed strong anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. These effects were exerted through the inhibition of the production of NO and pro-inflammatory cytokines, such as interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α). Furthermore, MPQP decreased the expression levels of inducible NO synthase (iNOS) and cyclooxygenase 2 (COX-2). Additionally, it mediated the inhibition of the phosphorylation of p38, c-Jun N-terminal kinase (JNK), the inhibitor of κBα (IκBα), and their upstream kinases, IκB kinase (IKK) α/β, mitogen-activated protein kinase kinase (MKK) 3/6, and MKK4. Furthermore, the expression of IL-1 receptor-associated kinase 1 (IRAK1) that regulates NF-κB, p38, and the JNK signaling pathways, was also increased by MPQP. These results indicate that MPQP regulates the IRAK1-mediated inflammatory signaling pathways by targeting IRAK1 or its upstream factors. [BMB Reports 2018; 51(6): 308-313].
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Cyclooxygenase 2/metabolism ; I-kappa B Proteins/metabolism ; Inflammation/drug therapy ; Interleukin-1 Receptor-Associated Kinases/antagonists & inhibitors ; Interleukin-1 Receptor-Associated Kinases/metabolism ; Lipopolysaccharides/pharmacology ; MAP Kinase Kinase 4/metabolism ; Macrophages/drug effects ; Mice ; NF-KappaB Inhibitor alpha/metabolism ; NF-kappa B/metabolism ; Nitric Oxide/biosynthesis ; Nitric Oxide/metabolism ; Phosphorylation/drug effects ; Quinolines/pharmacology ; RAW 264.7 Cells ; Signal Transduction/drug effects ; Small Molecule Libraries/pharmacology ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Anti-Inflammatory Agents ; I-kappa B Proteins ; Lipopolysaccharides ; NF-kappa B ; Quinolines ; Small Molecule Libraries ; NF-KappaB Inhibitor alpha (139874-52-5) ; Nitric Oxide (31C4KY9ESH) ; Cyclooxygenase 2 (EC 1.14.99.1) ; IRAK1 protein, human (EC 2.7.11.1) ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 4 (EC 2.7.12.2)
Language	English
Publishing date	2018-07-05
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2410389-5
ISSN	1976-670X ; 1976-6696
ISSN (online)	1976-670X
ISSN	1976-6696
DOI	10.5483/bmbrep.2018.51.6.064
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Suppression of inflammation by the rhizome of

Kim, Ba Reum / Cho, Young-Chang / Le, Hien Thi Thu / Vuong, Huong Lan / Lee, Sewoong / Cho, Sayeon

Biomedical reports

2017 Volume 6, Issue 6, Page(s) 691–697

Abstract: The rhizome ... ...

Abstract	The rhizome of
Language	English
Publishing date	2017-04-19
Publishing country	England
Document type	Journal Article
ZDB-ID	2763624-0
ISSN	2049-9442 ; 2049-9434
ISSN (online)	2049-9442
ISSN	2049-9434
DOI	10.3892/br.2017.895
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Article ; Online: Protein tyrosine phosphatase PTPN21 acts as a negative regulator of ICAM-1 by dephosphorylating IKKβ in TNF-α-stimulated human keratinocytes.

Cho, Young-Chang / Kim, Ba Reum / Cho, Sayeon

BMB reports

2017 Volume 50, Issue 11, Page(s) 584–589

Abstract: Intercellular adhesion molecule-1 (ICAM-1), which is induced by tumor necrosis factor (TNF)-α, contributes to the entry of immune cells into the site of inflammation in the skin. Here, we show that protein tyrosine phosphatase non-receptor type 21 ( ... ...

Abstract	Intercellular adhesion molecule-1 (ICAM-1), which is induced by tumor necrosis factor (TNF)-α, contributes to the entry of immune cells into the site of inflammation in the skin. Here, we show that protein tyrosine phosphatase non-receptor type 21 (PTPN21) negatively regulates ICAM-1 expression in human keratinocytes. PTPN21 expression was transiently induced after stimulation with TNF-α. When overexpressed, PTPN21 inhibited the expression of ICAM-1 in HaCaT cells but PTPN21 C1108S, a phosphatase activity-inactive mutant, failed to inhibit ICAM-1 expression. Nuclear factor-κB (NF-κB), a key transcription factor of ICAM-1 gene expression, was inhibited by PTPN21, but not by PTPN21 C1108S. PTPN21 directly dephosphorylated phospho-inhibitor of κB (IκB)-kinase β (IKKβ) at Ser177/181. This dephosphorylation led to the stabilization of IκBα and inhibition of NF-κB activity. Taken together, our results suggest that PTPN21 could be a valuable molecular target for regulation of inflammation in the skin by dephosphorylating p-IKKβ and inhibiting NF-κB signaling. [BMB Reports 2017; 50(11): 584-589].
MeSH term(s)	Cell Adhesion/drug effects ; Cell Line ; Gene Expression Regulation/drug effects ; Humans ; I-kappa B Kinase/metabolism ; I-kappa B Proteins/metabolism ; Intercellular Adhesion Molecule-1/metabolism ; Keratinocytes/metabolism ; Keratinocytes/pathology ; Mitogen-Activated Protein Kinases/metabolism ; NF-KappaB Inhibitor alpha/metabolism ; NF-kappa B/metabolism ; Phosphorylation ; Protein Tyrosine Phosphatases/metabolism ; Protein Tyrosine Phosphatases, Non-Receptor/metabolism ; Protein Tyrosine Phosphatases, Non-Receptor/physiology ; Signal Transduction/drug effects ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	I-kappa B Proteins ; NF-kappa B ; Tumor Necrosis Factor-alpha ; Intercellular Adhesion Molecule-1 (126547-89-5) ; NF-KappaB Inhibitor alpha (139874-52-5) ; I-kappa B Kinase (EC 2.7.11.10) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; PTPN21 protein, human (EC 3.1.3.48) ; Protein Tyrosine Phosphatases (EC 3.1.3.48) ; Protein Tyrosine Phosphatases, Non-Receptor (EC 3.1.3.48)
Language	English
Publishing date	2017-12-08
Publishing country	Korea (South)
Document type	News
ZDB-ID	2410389-5
ISSN	1976-670X ; 1976-6696
ISSN (online)	1976-670X
ISSN	1976-6696
DOI	10.5483/bmbrep.2017.50.11.169
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Article ; Online: Anti-cancer effects of ethanol extract of Reynoutria japonica Houtt. radix in human hepatocellular carcinoma cells via inhibition of MAPK and PI3K/Akt signaling pathways.

Kim, Ba Reum / Ha, Jain / Lee, Sewoong / Park, Jiyoung / Cho, Sayeon

Journal of ethnopharmacology

2019 Volume 245, Page(s) 112179

Abstract: Ethnopharmacological relevance: Reynoutria japonica Houtt. has been used as a traditional medicine of cancer in East Asia for thousands of years. However, the mechanism of the anti-cancer effect of R. japonica has not been investigated at the molecular ... ...

Abstract	Ethnopharmacological relevance: Reynoutria japonica Houtt. has been used as a traditional medicine of cancer in East Asia for thousands of years. However, the mechanism of the anti-cancer effect of R. japonica has not been investigated at the molecular level. The regulation of intracellular signaling pathways by the extract of R. japonica radix needs to be evaluated for a deeper understanding and application of the anti-cancer effect of R. japonica radix. Aim of the study: The purpose of this study was to evaluate the inhibitory effects of the ethanol extracts of R. japonica radix (ERJR) on cancer metastasis and the regulation mechanism of metastasis by ERJR in human hepatocellular carcinomas. Materials and methods: Suppression of cancer metastasis by ERJR in SK-Hep1 and Huh7 cells were investigated. Prior to experiments, the cytotoxic effect of ERJR was examined by cell viability assays. To evaluate the inhibitory effects of ERJR on cancer metastasis, wound-healing assays, invasion assays, zymography, and multicellular tumor spheroids (MCTS) assays were performed. Molecular mechanisms in the suppressive regulation of metastasis by ERJR were verified by measuring the expression levels of metastatic markers, and the phosphorylation and protein levels of cancer metastasis-related signaling pathways. Results: In all experiments, ERJR was used at a maximum concentration of 20 μg/ml, which did not show cytotoxicity in SK-Hep1 and Huh7 cells. We examined the inhibitory effects of ERJR on cancer metastasis. In wound-healing and invasion assays, ERJR treatment effectively suppressed the wound-recovery of Huh7 cells and inhibited the invasion ability of SK-Hep1 cells. Also, ERJR treatment significantly decreased the enzymatic activity of matrix metalloproteinase-2 and -9 in SK-Hep1 cells. ERJR suppressed the growth of MCTS in SK-Hep1 cells in a dose-dependent manner. These results indicated that ERJR effectively inhibited the invasive and proliferative ability of SK-Hep1 and Huh7 cells. Moreover, ERJR treatment reduced the expression levels of Snail1, Twist1, N-cadherin, and Vimentin, which are metastatic markers, by inhibiting the activation of protein kinase B and mitogen-activated protein kinases in SK-Hep1 cells. Conclusions: These results verified the molecular mechanism of ERJR that has been used in traditional anti-cancer remedy and suggest that it can be developed as a promising therapy for cancer metastasis in the future.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/metabolism ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Survival/drug effects ; Ethanol/chemistry ; Humans ; Liver Neoplasms/drug therapy ; Liver Neoplasms/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Plant Extracts/pharmacology ; Plant Roots/chemistry ; Polygonaceae ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects ; Solvents/chemistry ; Wound Healing/drug effects
Chemical Substances	Antineoplastic Agents ; Plant Extracts ; Solvents ; Ethanol (3K9958V90M) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2019-08-21
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2019.112179
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 1494: Show issues

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Article ; Online: Anti‑inflammatory effects on murine macrophages of ethanol extracts of Lygodium japonicum spores via inhibition of NF‑κB and p38.

Cho, Young-Chang / Kim, Ba Reum / Le, Hien Thi Thu / Cho, Sayeon

Molecular medicine reports

2017 Volume 16, Issue 4, Page(s) 4362–4370

Abstract: The spores of Lygodium japonicum (Thunb.) Sw. (L. japonicum) have been used in traditional Chinese medicine for the treatment of various inflammatory diseases. However, the molecular mechanisms underlying their anti‑inflammatory effects have yet to be ... ...

Abstract	The spores of Lygodium japonicum (Thunb.) Sw. (L. japonicum) have been used in traditional Chinese medicine for the treatment of various inflammatory diseases. However, the molecular mechanisms underlying their anti‑inflammatory effects have yet to be elucidated. In the present study, we investigated the anti‑inflammatory effects of ethanol extracts of L. japonicum spores (ELJ) by measuring the production of inflammatory mediators, and explored the molecular mechanisms underlying the effects of ELJ in murine macrophages in vitro using immunoblotting analyses. At non‑cytotoxic concentrations of (50‑300 µg/ml), ELJ was revealed to significantly suppress the production of nitric oxide (NO) and tumor necrosis factor (TNF)‑α in lipopolysaccharide (LPS)‑stimulated murine RAW 264.7 macrophages; ELJ repressed the production of interleukin (IL)‑6 only at high concentrations (≥200 µg/ml). The ELJ‑mediated decrease in NO production was demonstrated to depend on the downregulation of inducible NO synthase mRNA and protein expression. Conversely, the mRNA and protein expression of cyclooxygenase‑2 were not affected by ELJ. In addition, ELJ was revealed to inhibit the mRNA expression of IL‑6, IL‑1β, and TNF‑α in LPS‑stimulated RAW 264.7 macrophages. The effects of ELJ on proinflammatory mediators may have been due to the stabilization of inhibitor of κBα and the inhibition of p38 mitogen‑activated protein kinase (MAPK). These results suggested that ELJ may suppress LPS‑induced inflammatory responses in murine macrophages in vitro, through the negative regulation of p38 MAPK and nuclear factor (NF)‑κB. Therefore, ELJ may have potential as a novel candidate for the development of therapeutic strategies aimed at alleviating inflammation.
Language	English
Publishing date	2017-10
Publishing country	Greece
Document type	Journal Article
ISSN	1791-3004
ISSN (online)	1791-3004
DOI	10.3892/mmr.2017.7070
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Controlled formation of polylysinized inner pores in injectable microspheres of low molecular weight poly(lactide-co-glycolide) designed for efficient loading of therapeutic cells.

Kim, Hyeongmin / Kim, Ba Reum / Shin, Young Joo / Cho, Sayeon / Lee, Jaehwi

Artificial cells, nanomedicine, and biotechnology

2018 Volume 46, Issue sup3, Page(s) S233–S246

Abstract: This study aimed to develop porous microspheres with a suitable porous structure and mechanical property for cell delivery using a comparatively low molecular weight (MW) poly(lactide-co-glycolide) (PLGA) having a weak mechanical strength and fast ... ...

Abstract	This study aimed to develop porous microspheres with a suitable porous structure and mechanical property for cell delivery using a comparatively low molecular weight (MW) poly(lactide-co-glycolide) (PLGA) having a weak mechanical strength and fast degradation rate, which could be potentially used for treatment of corneal endothelial diseases. Porous microspheres of 30 kDa PLGA with different pore sizes were prepared by varying preparation conditions, and the microspheres with mean pore diameters approximately 0.5, 1, 2 and 3 times that of a single green fluorescent protein-expressing human embryonic kidney 293 cell, used as a model cell, were chosen for cell loading study. The microspheres with an average pore diameter two times greater than that of the single cell were found to be the most appropriate for efficient cell loading in the inner pore spaces, along with demonstrating a good mechanical property, injectability and biodegradability. To maximize the cell loading amount in the microspheres, the cell adhesive property of the microspheres and cell loading conditions were optimized, leading to approximately 4.2 times increase in the cell loading amount. The porous microspheres designed using the low MW PLGA hold promise as a delivery system of corneal endothelial cells for regeneration of the corneal endothelium.
MeSH term(s)	Cells, Immobilized/metabolism ; Cells, Immobilized/transplantation ; Cornea/blood supply ; Cornea/metabolism ; Cornea/pathology ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Endothelial Cells/transplantation ; Endothelium/metabolism ; Endothelium/pathology ; HEK293 Cells ; Humans ; Microspheres ; Polylactic Acid-Polyglycolic Acid Copolymer/chemistry ; Polylysine/chemistry ; Porosity
Chemical Substances	Polylactic Acid-Polyglycolic Acid Copolymer (1SIA8062RS) ; Polylysine (25104-18-1)
Language	English
Publishing date	2018-07-23
Publishing country	England
Document type	Journal Article
ZDB-ID	2723095-8
ISSN	2169-141X ; 2169-1401
ISSN (online)	2169-141X
ISSN	2169-1401
DOI	10.1080/21691401.2018.1491475
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Zs.A 1164: Show issues

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Article ; Online: Identification of a novel inhibitor of liver cancer cell invasion and proliferation through regulation of Akt and Twist1

Jain Ha / Sewoong Lee / Jiyoung Park / Jihye Seo / Eunjeong Kang / Haelim Yoon / Ba Reum Kim / Hyeon Kyu Lee / Seong Eon Ryu / Sayeon Cho

Scientific Reports, Vol 11, Iss 1, Pp 1-

2021 Volume 11

Abstract: Abstract When primary cancer faces limited oxygen and nutrient supply, it undergoes an epithelial–mesenchymal transition, which increases cancer cell motility and invasiveness. The migratory and invasive cancer cells often exert aggressive cancer ... ...

Abstract	Abstract When primary cancer faces limited oxygen and nutrient supply, it undergoes an epithelial–mesenchymal transition, which increases cancer cell motility and invasiveness. The migratory and invasive cancer cells often exert aggressive cancer development or even cancer metastasis. In this study, we investigated a novel compound, 3-acetyl-5,8-dichloro-2-((2,4-dichlorophenyl)amino)quinolin-4(1H)-one (ADQ), that showed significant suppression of wound healing and cellular invasion. This compound also inhibited anchorage-independent cell growth, multicellular tumor spheroid survival/invasion, and metalloprotease activities. The anti-proliferative effects of ADQ were mediated by inhibition of the Akt pathway. In addition, ADQ reduced the expression of mesenchymal markers of cancer cells, which was associated with the suppressed expression of Twist1. In conclusion, ADQ successfully suppressed carcinogenic activity by inhibiting the Akt signaling pathway and Twist1, which suggests that ADQ may be an efficient candidate for cancer drug development.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2021-08-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Identification of a novel inhibitor of liver cancer cell invasion and proliferation through regulation of Akt and Twist1.

Ha, Jain / Lee, Sewoong / Park, Jiyoung / Seo, Jihye / Kang, Eunjeong / Yoon, Haelim / Kim, Ba Reum / Lee, Hyeon Kyu / Ryu, Seong Eon / Cho, Sayeon

Scientific reports

2021 Volume 11, Issue 1, Page(s) 16765

Abstract: When primary cancer faces limited oxygen and nutrient supply, it undergoes an epithelial-mesenchymal transition, which increases cancer cell motility and invasiveness. The migratory and invasive cancer cells often exert aggressive cancer development or ... ...

Abstract	When primary cancer faces limited oxygen and nutrient supply, it undergoes an epithelial-mesenchymal transition, which increases cancer cell motility and invasiveness. The migratory and invasive cancer cells often exert aggressive cancer development or even cancer metastasis. In this study, we investigated a novel compound, 3-acetyl-5,8-dichloro-2-((2,4-dichlorophenyl)amino)quinolin-4(1H)-one (ADQ), that showed significant suppression of wound healing and cellular invasion. This compound also inhibited anchorage-independent cell growth, multicellular tumor spheroid survival/invasion, and metalloprotease activities. The anti-proliferative effects of ADQ were mediated by inhibition of the Akt pathway. In addition, ADQ reduced the expression of mesenchymal markers of cancer cells, which was associated with the suppressed expression of Twist1. In conclusion, ADQ successfully suppressed carcinogenic activity by inhibiting the Akt signaling pathway and Twist1, which suggests that ADQ may be an efficient candidate for cancer drug development.
MeSH term(s)	Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; Humans ; Liver Neoplasms/drug therapy ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Neoplasm Invasiveness ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Twist-Related Protein 1/genetics ; Twist-Related Protein 1/metabolism
Chemical Substances	Antineoplastic Agents ; Nuclear Proteins ; TWIST1 protein, human ; Twist-Related Protein 1 ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2021-08-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-95933-4
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Spilanthes acmella inhibits inflammatory responses via inhibition of NF-κB and MAPK signaling pathways in RAW 264.7 macrophages.

Cho, Young-Chang / Bach, Tran The / Kim, Ba Reum / Vuong, Huong Lan / Cho, Sayeon

Molecular medicine reports

2017 Volume 16, Issue 1, Page(s) 339–346

Abstract: Spilanthes acmella Murr. (S. acmella) has been used traditionally in India and Sri Lanka to treat various inflammatory diseases. However, the anti‑inflammatory effects and underlying mechanism of action of S. acmella are unclear. The present study ... ...

Abstract	Spilanthes acmella Murr. (S. acmella) has been used traditionally in India and Sri Lanka to treat various inflammatory diseases. However, the anti‑inflammatory effects and underlying mechanism of action of S. acmella are unclear. The present study assessed the anti‑inflammatory properties of methanol extracts of S. acmella (MSA) in murine macrophages. MSA (≤300 µg/ml) inhibited nitric oxide (NO) production in lipopolysaccharide (LPS)‑stimulated RAW 264.7 macrophages through transcriptional inhibition of inducible nitric oxide synthase expression in a dose‑dependent manner. Furthermore, the LPS‑induced prostaglandin E2 production and cyclooxygenase‑2 expression were inhibited by MSA (300 µg/ml). MSA treatment inhibited interleukin (IL)‑6 production and decreased the mRNA expression levels of proinflammatory cytokines, including IL‑6 and IL‑1β. In addition, no significant inhibition in tumor necrosis factor‑α production was detected. Inhibitory effects of MSA on the production of inflammatory mediators were mediated by reduced activation of mitogen‑activated protein kinases (MAPKs) and nuclear factor (NF)‑κB. The LPS‑induced phosphorylation of transforming growth factor beta‑activated kinase 1, an upstream kinase of both MAPKs and NF‑κB, was also inhibited by MSA treatment. Taken together, MSA inhibits the excessive inflammatory responses in LPS‑stimulated murine macrophages by inhibiting the phosphorylation of MAPKs and NF‑κB, implicating S. acmella in the treatment of severe inflammatory states based on its ethnopharmacological importance and its anti‑inflammatory properties.
Language	English
Publishing date	2017-07
Publishing country	Greece
Document type	Journal Article
ISSN	1791-3004
ISSN (online)	1791-3004
DOI	10.3892/mmr.2017.6555
Database	MEDical Literature Analysis and Retrieval System OnLINE

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