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  1. AU="Viswanadha, Vijaya P"
  2. AU="Anastasi, G A"
  3. AU="Romerosa, Antonio"
  4. AU=Gupta Gaorav P
  5. AU="Fernández-Susavila, Héctor"

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  1. Article ; Online: Lipoxygenase (LOX) Pathway: A Promising Target to Combat Cancer.

    Vishnupriya, P / Aparna, A / Viswanadha, Vijaya P

    Current pharmaceutical design

    2020  Volume 27, Issue 31, Page(s) 3349–3369

    Abstract: Leukotrienes are one of the major eicosanoid lipid mediators produced due to an oxidative transformation of arachidonic acid. Subsequently, they get converted into various cellular signaling hormones by a series of enzymes of myeloid origin to mediate or ...

    Abstract Leukotrienes are one of the major eicosanoid lipid mediators produced due to an oxidative transformation of arachidonic acid. Subsequently, they get converted into various cellular signaling hormones by a series of enzymes of myeloid origin to mediate or debilitate inflammation. Interestingly, the available literature demonstrates the pivotal role of eicosanoids in neurodegenerative, obesity, diabetes, cardiovascular diseases, and cancers as well. The aberrant metabolism of arachidonic acid by the LOX pathway is a common feature of epithelial-derived malignancies and suggests the contributory role of dietary fats in carcinogenesis. The enzymes and receptors of the LOX pathway play a significant role in cell proliferation, differentiation and regulation of apoptosis through multiple signaling pathways and have been reported to be involved in various cancers, including prostate, colon, lung and pancreatic cancers. So far, leukotriene receptor antagonists and 5-LOX inhibitors have reached up to the clinical trials for treating various diseases. Keeping its various roles in cancer, the review highlights the components of the leukotriene synthesizing machinery, emerging opportunities for pharmacological intervention, and the probability of considering lipoxygenases and leukotriene receptors as good candidates for clinical chemoprevention studies.
    MeSH term(s) Humans ; Leukotrienes/metabolism ; Lipid Metabolism ; Lipoxygenases/metabolism ; Male ; Pancreatic Neoplasms ; Signal Transduction
    Chemical Substances Leukotrienes ; Lipoxygenases (EC 1.13.11.-)
    Language English
    Publishing date 2020-12-30
    Publishing country United Arab Emirates
    Document type Journal Article
    ZDB-ID 1304236-1
    ISSN 1873-4286 ; 1381-6128
    ISSN (online) 1873-4286
    ISSN 1381-6128
    DOI 10.2174/1381612826666210101153216
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4714: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
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  2. Article ; Online: Protective effects of luteolin against oxidative stress and mitochondrial dysfunction in endothelial cells.

    Chen, Hsiu-I / Hu, Wei-Syun / Hung, Meng-Yu / Ou, Hsiu-Chung / Huang, Su-Hua / Hsu, Pei-Tzu / Day, Cecilia-Hsuan / Lin, Kuan-Ho / Viswanadha, Vijaya P / Kuo, Wei-Wen / Huang, Chih-Yang

    Nutrition, metabolism, and cardiovascular diseases : NMCD

    2020  Volume 30, Issue 6, Page(s) 1032–1043

    Abstract: Background and aims: Luteolin is a common flavonoid that is abundantly present in various edible plants, it is known to exhibit beneficial effects on cardiovascular system. However, the mechanisms which underlie the protective effects of luteolin on ... ...

    Abstract Background and aims: Luteolin is a common flavonoid that is abundantly present in various edible plants, it is known to exhibit beneficial effects on cardiovascular system. However, the mechanisms which underlie the protective effects of luteolin on endothelial cell damage caused by oxidative stress remains unclear. The purpose of this study is to test the hypothesis which states that luteolin protects against H
    Methods and results: Human umbilical vein endothelial cells (HUVECs) were pretreated with luteolin prior to being stimulated by 600 μM H
    Conclusion: Results from this study may provide the possible molecular mechanisms underlying cardiovascular protective effects of luteolin.
    MeSH term(s) Antioxidants/pharmacology ; Apoptosis/drug effects ; Calcium Signaling/drug effects ; Cells, Cultured ; Human Umbilical Vein Endothelial Cells/drug effects ; Human Umbilical Vein Endothelial Cells/metabolism ; Human Umbilical Vein Endothelial Cells/pathology ; Humans ; Hydrogen Peroxide/toxicity ; Luteolin/pharmacology ; Membrane Potential, Mitochondrial/drug effects ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/pathology ; NF-kappa B/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Nitric Oxide Synthase Type III/metabolism ; Oxidative Stress/drug effects ; Phosphorylation ; Reactive Oxygen Species/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances Antioxidants ; NF-kappa B ; Reactive Oxygen Species ; Hydrogen Peroxide (BBX060AN9V) ; NOS2 protein, human (EC 1.14.13.39) ; NOS3 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Luteolin (KUX1ZNC9J2)
    Language English
    Publishing date 2020-03-09
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1067704-5
    ISSN 1590-3729 ; 0939-4753
    ISSN (online) 1590-3729
    ISSN 0939-4753
    DOI 10.1016/j.numecd.2020.02.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3149: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article: Fisetin activates Hippo pathway and JNK/ERK/AP‐1 signaling to inhibit proliferation and induce apoptosis of human osteosarcoma cells via ZAK overexpression

    Fu, Chien‐Yao / Chen, Mei‐Chih / Chen, Ming‐Cheng / Huang, Chih‐Yang / Lin, Yueh‐Min / Tseng, Yan‐Shen / Viswanadha, Vijaya P / Wang, Guiqing / Yang, Jaw‐Ji / Zhou, Zhengtao

    Environmental toxicology. 2019 Aug., v. 34, no. 8

    2019  

    Abstract: Osteosarcoma (OS) is a tumor entity that can cause a large number of cancer‐related deaths. Although chemotherapy can decrease proliferation and increase apoptosis of human OS cells, the clinical prognosis remains poor. Fisetin is a flavonol found in ... ...

    Abstract Osteosarcoma (OS) is a tumor entity that can cause a large number of cancer‐related deaths. Although chemotherapy can decrease proliferation and increase apoptosis of human OS cells, the clinical prognosis remains poor. Fisetin is a flavonol found in fruits and vegetables and is reported to inhibit cell growth in numerous cancers. But the molecular mechanism underlying fisetin in human OS cells is not clear. It is known that sterile‐alpha motif and leucine zipper containing kinase (ZAK), a kinase in the MAP3K family, is involved in various cell processes, including proliferation and apoptosis. In our lab, we have demonstrated that overexpression of ZAK can induce apoptosis in human OS cells. In the previous studies, MAP4K, the upstream of MAP3K, can act in parallel to MST1/2 to activate LATS1/2 in the Hippo pathway. Turning on the Hippo pathway can decrease proliferation and otherwise cause cell apoptosis in cancer cells. In this study, we found that fisetin can upregulate ZAK expression to induce the Hippo pathway and mediate the activation of JNK/ERK, the downstream of ZAK, to trigger cell apoptosis via AP‐1 dependent manner in human OS cells. These findings reveal a novel molecular mechanism underlying fisetin effect on human OS cells.
    Keywords apoptosis ; cell growth ; drug therapy ; flavonols ; fruits ; humans ; leucine zipper ; mitogen-activated protein kinase ; mitogen-activated protein kinase kinase kinase ; neoplasm cells ; osteosarcoma ; prognosis ; vegetables
    Language English
    Dates of publication 2019-08
    Size p. 902-911.
    Publishing place John Wiley & Sons, Inc.
    Document type Article
    Note JOURNAL ARTICLE
    ZDB-ID 1463449-1
    ISSN 1522-7278 ; 1520-4081
    ISSN (online) 1522-7278
    ISSN 1520-4081
    DOI 10.1002/tox.22761
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 4957: Show issues

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  4. Article ; Online: Tid1-S attenuates LPS-induced cardiac hypertrophy and apoptosis through ER-a mediated modulation of p-PI3K/p-Akt signaling cascade.

    Chao, Chun-Nun / Lo, Jeng-Fan / Khan, Farheen B / Day, Cecilia H / Lai, Chao-Hung / Chen, Chia-Hua / Chen, Ray-Jade / Viswanadha, Vijaya P / Kuo, Chia-Hua / Huang, Chih-Yang

    Journal of cellular biochemistry

    2019  Volume 120, Issue 10, Page(s) 16703–16710

    Abstract: Myocardial dysfunction is clinically relevant? repercussion that follows sepsis. Tid 1 protein has been implicated in many biological process. However, the role of Tid 1 in lipopolysaccharide (LPS)-induced cardiomyocyte hypertrophy and apoptosis remains ... ...

    Abstract Myocardial dysfunction is clinically relevant? repercussion that follows sepsis. Tid 1 protein has been implicated in many biological process. However, the role of Tid 1 in lipopolysaccharide (LPS)-induced cardiomyocyte hypertrophy and apoptosis remains elusive. In the current research endeavor, we have elucidated the role of Tid1-S on LPS-induced cardiac hypertrophy and apoptosis. Interestingly, we found that overexpression of Tid1-S suppressed TLR-4, NFATc3, and BNP protein expression which eventually led to inhibition of LPS-induced cardiac hypertrophy. Moreover, Tid1-S overexpression attenuated cellular apoptosis and activated survival proteins p-PI3K and p
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Animals ; Apoptosis/drug effects ; Cardiomegaly/chemically induced ; Cardiomegaly/metabolism ; Cardiomegaly/pathology ; Estrogen Receptor alpha/metabolism ; Female ; Gene Expression Regulation/drug effects ; HSP40 Heat-Shock Proteins/metabolism ; Humans ; Lipopolysaccharides/toxicity ; Male ; Middle Aged ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Signal Transduction/drug effects
    Chemical Substances DNAJA3 protein, human ; ESR1 protein, human ; Estrogen Receptor alpha ; HSP40 Heat-Shock Proteins ; Lipopolysaccharides ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2019-05-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 392402-6
    ISSN 1097-4644 ; 0730-2312
    ISSN (online) 1097-4644
    ISSN 0730-2312
    DOI 10.1002/jcb.28928
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1114: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Fisetin activates Hippo pathway and JNK/ERK/AP-1 signaling to inhibit proliferation and induce apoptosis of human osteosarcoma cells via ZAK overexpression.

    Fu, Chien-Yao / Chen, Mei-Chih / Tseng, Yan-Shen / Chen, Ming-Cheng / Zhou, Zhengtao / Yang, Jaw-Ji / Lin, Yueh-Min / Viswanadha, Vijaya P / Wang, Guiqing / Huang, Chih-Yang

    Environmental toxicology

    2019  Volume 34, Issue 8, Page(s) 902–911

    Abstract: Osteosarcoma (OS) is a tumor entity that can cause a large number of cancer-related deaths. Although chemotherapy can decrease proliferation and increase apoptosis of human OS cells, the clinical prognosis remains poor. Fisetin is a flavonol found in ... ...

    Abstract Osteosarcoma (OS) is a tumor entity that can cause a large number of cancer-related deaths. Although chemotherapy can decrease proliferation and increase apoptosis of human OS cells, the clinical prognosis remains poor. Fisetin is a flavonol found in fruits and vegetables and is reported to inhibit cell growth in numerous cancers. But the molecular mechanism underlying fisetin in human OS cells is not clear. It is known that sterile-alpha motif and leucine zipper containing kinase (ZAK), a kinase in the MAP3K family, is involved in various cell processes, including proliferation and apoptosis. In our lab, we have demonstrated that overexpression of ZAK can induce apoptosis in human OS cells. In the previous studies, MAP4K, the upstream of MAP3K, can act in parallel to MST1/2 to activate LATS1/2 in the Hippo pathway. Turning on the Hippo pathway can decrease proliferation and otherwise cause cell apoptosis in cancer cells. In this study, we found that fisetin can upregulate ZAK expression to induce the Hippo pathway and mediate the activation of JNK/ERK, the downstream of ZAK, to trigger cell apoptosis via AP-1 dependent manner in human OS cells. These findings reveal a novel molecular mechanism underlying fisetin effect on human OS cells.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Apoptosis ; Bone Neoplasms/enzymology ; Bone Neoplasms/metabolism ; Bone Neoplasms/pathology ; Cell Line, Tumor ; Cell Proliferation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Flavonoids/pharmacology ; Humans ; JNK Mitogen-Activated Protein Kinases/metabolism ; MAP Kinase Kinase Kinases ; MAP Kinase Signaling System ; Osteosarcoma/enzymology ; Osteosarcoma/metabolism ; Osteosarcoma/pathology ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; Transcription Factor AP-1/metabolism ; Tumor Suppressor Proteins/metabolism
    Chemical Substances Antineoplastic Agents ; Flavonoids ; Transcription Factor AP-1 ; Tumor Suppressor Proteins ; Protein Kinases (EC 2.7.-) ; LATS2 protein, human (EC 2.7.1.11) ; Hippo protein, human (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP3K20 protein, human (EC 2.7.11.25) ; fisetin (OO2ABO9578)
    Language English
    Publishing date 2019-05-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1463449-1
    ISSN 1522-7278 ; 1520-4081
    ISSN (online) 1522-7278
    ISSN 1520-4081
    DOI 10.1002/tox.22761
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2676: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: The multifaceted link between inflammation and human diseases.

    Rajendran, Peramaiyan / Chen, Ya-Fang / Chen, Yu-Feng / Chung, Li-Chin / Tamilselvi, Shanmugam / Shen, Chia-Yao / Day, Cecilia Hsuan / Chen, Ray-Jade / Viswanadha, Vijaya P / Kuo, Wei-Wen / Huang, Chih-Yang

    Journal of cellular physiology

    2018  Volume 233, Issue 9, Page(s) 6458–6471

    Abstract: Increasing reports on epidemiological, diagnostic, and clinical studies suggest that dysfunction of the inflammatory reaction results in chronic illnesses such as cancer, arthritis, arteriosclerosis, neurological disorders, liver diseases, and renal ... ...

    Abstract Increasing reports on epidemiological, diagnostic, and clinical studies suggest that dysfunction of the inflammatory reaction results in chronic illnesses such as cancer, arthritis, arteriosclerosis, neurological disorders, liver diseases, and renal disorders. Chronic inflammation might progress if injurious agent persists; however, more typically than not, the response is chronic from the start. Distinct to most changes in acute inflammation, chronic inflammation is characterized by the infiltration of damaged tissue by mononuclear cells like macrophages, lymphocytes, and plasma cells, in addition to tissue destruction and attempts to repair. Phagocytes are the key players in the chronic inflammatory response. However, the important drawback is the activation of pathological phagocytes, which might result from continued tissue damage and lead to harmful diseases. The longer the inflammation persists, the greater the chance for the establishment of human diseases. The aim of this review was to focus on advances in the understanding of chronic inflammation and to summarize the impact and involvement of inflammatory agents in certain human diseases.
    MeSH term(s) Animals ; Chronic Disease ; Humans ; Inflammation/pathology ; Leukocytes, Mononuclear/pathology ; Phagocytes/pathology
    Language English
    Publishing date 2018-03-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.26479
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.212: Show issues Location:
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