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  1. AU="Herůdková, Jarmila"
  2. AU="Jacob, Jeku"

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  1. Article ; Online: Inhibition of Chk1 stimulates cytotoxic action of platinum-based drugs and TRAIL combination in human prostate cancer cells.

    Krkoška, Martin / Paruch, Kamil / Šošolíková, Tereza / Vázquez-Gómez, Gerardo / Herůdková, Jarmila / Novotný, Jan / Ovesná, Petra / Sova, Petr / Hyršlová Vaculová, Alena

    Biological chemistry

    2024  

    Abstract: Checkpoint kinase 1 (Chk1) plays an important role in regulation of the cell cycle, DNA damage response and cell death, and represents an attractive target in anticancer therapy. Small-molecule inhibitors of Chk1 have been intensively investigated either ...

    Abstract Checkpoint kinase 1 (Chk1) plays an important role in regulation of the cell cycle, DNA damage response and cell death, and represents an attractive target in anticancer therapy. Small-molecule inhibitors of Chk1 have been intensively investigated either as single agents or in combination with various chemotherapeutic drugs and they can enhance the chemosensitivity of numerous tumor types. Here we newly demonstrate that pharmacological inhibition of Chk1 using potent and selective inhibitor SCH900776, currently profiled in phase II clinical trials, significantly enhances cytotoxic effects of the combination of platinum-based drugs (cisplatin or LA-12) and TRAIL (tumor necrosis factor-related apoptosis inducing ligand) in human prostate cancer cells. The specific role of Chk1 in the drug combination-induced cytotoxicity was confirmed by siRNA-mediated silencing of this kinase. Using RNAi-based methods we also showed the importance of Bak-dependent mitochondrial apoptotic pathway in the combined anticancer action of SCH900776, cisplatin and TRAIL. The triple drug combination-induced cytotoxicity was partially enhanced by siRNA-mediated Mcl-1 silencing. Our findings suggest that targeting Chk1 may be used as an efficient strategy for sensitization of prostate cancer cells to killing action of platinum-based chemotherapeutic drugs and TRAIL.
    Language English
    Publishing date 2024-03-08
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1334659-3
    ISSN 1437-4315 ; 1431-6730 ; 1432-0355
    ISSN (online) 1437-4315
    ISSN 1431-6730 ; 1432-0355
    DOI 10.1515/hsz-2023-0111
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Role of miR-653 and miR-29c in downregulation of CYP1A2 expression in hepatocellular carcinoma.

    Krkoška, Martin / Nekvindová, Jana / Nevědělová, Kateřina / Zubáňová, Veronika / Radová, Lenka / Vondráček, Jan / Herůdková, Jarmila / Slabý, Ondřej / Kiss, Igor / Bohovicová, Lucia / Fabian, Pavel / Tylichová, Zuzana / Kala, Zdeněk / Kysela, Petr / Ostřížková, Lenka / Palička, Vladimír / Hyršlová Vaculová, Alena

    Pharmacological reports : PR

    2021  Volume 74, Issue 1, Page(s) 148–158

    Abstract: Background: Hepatocellular carcinoma (HCC) is a major contributor to the worldwide cancer burden. Recent studies on HCC have demonstrated dramatic alterations in expression of several cytochrome P450 (CYP) family members that play a crucial role in ... ...

    Abstract Background: Hepatocellular carcinoma (HCC) is a major contributor to the worldwide cancer burden. Recent studies on HCC have demonstrated dramatic alterations in expression of several cytochrome P450 (CYP) family members that play a crucial role in biotransformation of many drugs and other xenobiotics; however, the mechanisms responsible for their deregulation remain unclear.
    Methods: We investigated a potential involvement of miRNAs in downregulation of expression of CYPs observed in HCC tumors. We compared miRNA expression profiles (TaqMan Array Human MicroRNA v3.0 TLDA qPCR) between HCC human patient tumors with strong (CYP-) and weak/no (CYP+) downregulation of drug-metabolizing CYPs. The role of significantly deregulated miRNAs in modulation of expression of the CYPs and associated xenobiotic receptors was then investigated in human liver HepaRG cells transfected with relevant miRNA mimics or inhibitors.
    Results: We identified five differentially expressed miRNAs in CYP- versus CYP+ tumors, namely miR-29c, miR-125b1, miR-505, miR-653 and miR-675. The two most-upregulated miRNAs found in CYP- tumor samples, miR-29c and miR-653, were found to act as efficient suppressors of CYP1A2 or AHR expression.
    Conclusions: Our results revealed a novel role of miR-653 and miR-29c in regulation of expresion of CYPs involved in crucial biotransformation processes in liver, which are often deregulated during liver cancer progression.
    MeSH term(s) Biotransformation ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Cell Line, Tumor ; Cytochrome P-450 CYP1A2/metabolism ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Hepatocytes/metabolism ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; MicroRNAs/metabolism ; Xenobiotics/metabolism
    Chemical Substances MIRN29C microRNA, human ; MIRN653 microRNA, human ; MicroRNAs ; Xenobiotics ; CYP1A2 protein, human (EC 1.14.14.1) ; Cytochrome P-450 CYP1A2 (EC 1.14.14.1)
    Language English
    Publishing date 2021-11-15
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2186248-5
    ISSN 1734-1140
    ISSN 1734-1140
    DOI 10.1007/s43440-021-00338-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Chk1 Inhibitor SCH900776 Effectively Potentiates the Cytotoxic Effects of Platinum-Based Chemotherapeutic Drugs in Human Colon Cancer Cells.

    Herůdková, Jarmila / Paruch, Kamil / Khirsariya, Prashant / Souček, Karel / Krkoška, Martin / Vondálová Blanářová, Olga / Sova, Petr / Kozubík, Alois / Hyršlová Vaculová, Alena

    Neoplasia (New York, N.Y.)

    2017  Volume 19, Issue 10, Page(s) 830–841

    Abstract: Although Chk1 kinase inhibitors are currently under clinical investigation as effective cancer cell sensitizers to the cytotoxic effects of numerous chemotherapeutics, there is still a considerable uncertainty regarding their role in modulation of ... ...

    Abstract Although Chk1 kinase inhibitors are currently under clinical investigation as effective cancer cell sensitizers to the cytotoxic effects of numerous chemotherapeutics, there is still a considerable uncertainty regarding their role in modulation of anticancer potential of platinum-based drugs. Here we newly demonstrate the ability of one of the most specific Chk1 inhibitors, SCH900776 (MK-8776), to enhance human colon cancer cell sensitivity to the cytotoxic effects of platinum(II) cisplatin and platinum(IV)- LA-12 complexes. The combined treatment with SCH900776 and cisplatin or LA-12 results in apparent increase in G1/S phase-related apoptosis, stimulation of mitotic slippage, and senescence of HCT116 cells. We further show that the cancer cell response to the drug combinations is significantly affected by the p21, p53, and PTEN status. In contrast to their wt counterparts, the p53- or p21-deficient cells treated with SCH900776 and cisplatin or LA-12 enter mitosis and become polyploid, and the senescence phenotype is strongly suppressed. While the cell death induced by SCH900776 and cisplatin or LA-12 is significantly delayed in the absence of p53, the anticancer action of the drug combinations is significantly accelerated in p21-deficient cells, which is associated with stimulation of apoptosis beyond G2/M cell cycle phase. We also show that cooperative killing action of the drug combinations in HCT116 cells is facilitated in the absence of PTEN. Our results indicate that SCH900776 may act as an important modulator of cytotoxic response triggered by platinum-based drugs in colon cancer cells.
    Language English
    Publishing date 2017-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1483840-0
    ISSN 1476-5586 ; 1522-8002
    ISSN (online) 1476-5586
    ISSN 1522-8002
    DOI 10.1016/j.neo.2017.08.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  4. Article ; Online: Cisplatin or LA-12 enhance killing effects of TRAIL in prostate cancer cells through Bid-dependent stimulation of mitochondrial apoptotic pathway but not caspase-10.

    Vondálová Blanářová, Olga / Šafaříková, Barbora / Herůdková, Jarmila / Krkoška, Martin / Tománková, Silvie / Kahounová, Zuzana / Anděra, Ladislav / Bouchal, Jan / Kharaishvili, Gvantsa / Král, Milan / Sova, Petr / Kozubík, Alois / Hyršlová Vaculová, Alena

    PloS one

    2017  Volume 12, Issue 11, Page(s) e0188584

    Abstract: Searching for new strategies for effective elimination of human prostate cancer cells, we investigated the cooperative cytotoxic action of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and two platinum-based complexes, cisplatin or LA- ... ...

    Abstract Searching for new strategies for effective elimination of human prostate cancer cells, we investigated the cooperative cytotoxic action of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and two platinum-based complexes, cisplatin or LA-12, and related molecular mechanisms. We demonstrated a notable ability of cisplatin or LA-12 to enhance the sensitivity of several human prostate cancer cell lines to TRAIL-induced cell death via an engagement of mitochondrial apoptotic pathway. This was accompanied by augmented Bid cleavage, Bak activation, loss of mitochondrial membrane potential, activation of caspase-8, -10, -9, and -3, and XIAP cleavage. RNAi-mediated silencing of Bid or Bak in Bax-deficient DU 145 cells suppressed the drug combination-induced cytotoxicity, further underscoring the involvement of mitochondrial signaling. The caspase-10 was dispensable for enhancement of cisplatin/LA-12 and TRAIL combination-induced cell death and stimulation of Bid cleavage. Importantly, we newly demonstrated LA-12-mediated enhancement of TRAIL-induced cell death in cancer cells derived from human patient prostate tumor specimens. Our results provide convincing evidence that employing TRAIL combined with cisplatin/LA-12 could contribute to more effective killing of prostate cancer cells compared to the individual action of the drugs, and offer new mechanistic insights into their cooperative anticancer action.
    MeSH term(s) Amantadine/analogs & derivatives ; Amantadine/pharmacology ; Apoptosis/drug effects ; BH3 Interacting Domain Death Agonist Protein/metabolism ; Caspase 10/metabolism ; Cisplatin/pharmacology ; Humans ; Male ; Mitochondria/drug effects ; Mitochondria/metabolism ; Organoplatinum Compounds/pharmacology ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; TNF-Related Apoptosis-Inducing Ligand/metabolism
    Chemical Substances BH3 Interacting Domain Death Agonist Protein ; BID protein, human ; Organoplatinum Compounds ; TNF-Related Apoptosis-Inducing Ligand ; bis(acetato)(1-adamantylamine)amminedichloroplatinum(IV) ; Amantadine (BF4C9Z1J53) ; Caspase 10 (EC 3.4.22.-) ; Cisplatin (Q20Q21Q62J)
    Language English
    Publishing date 2017
    Publishing country United States
    Document type Journal Article
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0188584
    Database MEDical Literature Analysis and Retrieval System OnLINE

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