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  1. Article ; Online: Neuroprotective effect of zolpidem against glutamate-induced toxicity is mediated via the PI3K/Akt pathway and inhibited by PK11195.

    Jazvinšćak Jembrek, Maja / Radovanović, Vedrana / Vlainić, Josipa / Vuković, Lidija / Hanžić, Nikolina

    Toxicology

    2018  Volume 406-407, Page(s) 58–69

    Abstract: Excitotoxicity is a pathological process in which neuronal dysfunction and death are induced by excessive glutamate stimulation, the major fast excitatory neurotransmitter in the mammalian brain. Excitotoxicity-induced neurodegeneration is a contributing ...

    Abstract Excitotoxicity is a pathological process in which neuronal dysfunction and death are induced by excessive glutamate stimulation, the major fast excitatory neurotransmitter in the mammalian brain. Excitotoxicity-induced neurodegeneration is a contributing factor in ischemia-induced brain damage, traumatic brain injury, and various neurodegenerative diseases. It is triggered by calcium overload due to prolonged over-activation of ionotropic N-methyl-d-aspartate (NMDA) receptors. Enhanced Ca
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Dose-Response Relationship, Drug ; GABA Antagonists/pharmacology ; GABA-A Receptor Agonists/pharmacology ; Glutamic Acid/toxicity ; Isoquinolines/pharmacology ; Mice ; Neuroprotective Agents/pharmacology ; Phosphatidylinositol 3-Kinase/physiology ; Proto-Oncogene Proteins c-akt/physiology ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Treatment Outcome ; Zolpidem/pharmacology
    Chemical Substances Antineoplastic Agents ; GABA Antagonists ; GABA-A Receptor Agonists ; Isoquinolines ; Neuroprotective Agents ; Glutamic Acid (3KX376GY7L) ; Zolpidem (7K383OQI23) ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; PK 11195 (YNF83VN1RL)
    Language English
    Publishing date 2018-05-30
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 184557-3
    ISSN 1879-3185 ; 0300-483X
    ISSN (online) 1879-3185
    ISSN 0300-483X
    DOI 10.1016/j.tox.2018.05.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Neurotoxic Effect of Ethanolic Extract of Propolis in the Presence of Copper Ions is Mediated through Enhanced Production of ROS and Stimulation of caspase-3/7 Activity.

    Radovanović, Vedrana / Vlainić, Josipa / Hanžić, Nikolina / Ukić, Petra / Oršolić, Nada / Baranović, Goran / Jazvinšćak Jembrek, Maja

    Toxins

    2019  Volume 11, Issue 5

    Abstract: Elevated amounts of copper are considered to be contributing factor in the progression of neurodegenerative diseases as they promote oxidative stress conditions. The aim of our study was to examine the effects of ethanolic extract of propolis (EEP) ... ...

    Abstract Elevated amounts of copper are considered to be contributing factor in the progression of neurodegenerative diseases as they promote oxidative stress conditions. The aim of our study was to examine the effects of ethanolic extract of propolis (EEP) against copper-induced neuronal damage. In cultured P19 neuronal cells, EEP exacerbated copper-provoked neuronal cell death by increasing the generation of reactive oxygen species (ROS) and through the activation of caspase-3/7 activity. EEP augmented copper-induced up-regulation of p53 and Bax mRNA expressions. Neurotoxic effects of EEP were accompanied by a strong induction of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) expression and decrease in the expression of c-fos mRNA. SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK) prevented detrimental effects of EEP, whereas SP600125, an inhibitor of c-Jun N-terminal kinase (JNK), exacerbated EEP-induced neuronal cell death. Quercetin, a polyphenolic nutraceutical, which is usually present in propolis, was also able to exacerbate copper-induced neuronal death. Our data indicates a pro-oxidative and apoptotic mode of EEP action in the presence of excess copper, wherein ROS/p53/p38 interactions play an important role in death cascades. Our study also pointed out that detailed pharmacological and toxicological studies must be carried out for propolis and other dietary supplements in order to fully recognize the potential adverse effects in specific conditions.
    MeSH term(s) Animals ; Caspase 3/metabolism ; Caspase 7/metabolism ; Cell Line ; Cell Survival/drug effects ; Complex Mixtures/toxicity ; Copper/toxicity ; Ethanol/chemistry ; Mice ; Neurons/drug effects ; Neurons/metabolism ; Neurotoxins/toxicity ; Propolis/chemistry ; Reactive Oxygen Species/metabolism ; Solvents/chemistry ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances Complex Mixtures ; Neurotoxins ; Reactive Oxygen Species ; Solvents ; Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; Ethanol (3K9958V90M) ; Copper (789U1901C5) ; Propolis (9009-62-5) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Caspase 3 (EC 3.4.22.-) ; Caspase 7 (EC 3.4.22.-)
    Language English
    Publishing date 2019-05-15
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518395-3
    ISSN 2072-6651 ; 2072-6651
    ISSN (online) 2072-6651
    ISSN 2072-6651
    DOI 10.3390/toxins11050273
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Altered Expression of Shorter p53 Family Isoforms Can Impact Melanoma Aggressiveness.

    Tadijan, Ana / Precazzini, Francesca / Hanžić, Nikolina / Radić, Martina / Gavioli, Nicolò / Vlašić, Ignacija / Ozretić, Petar / Pinto, Lia / Škreblin, Lidija / Barban, Giulia / Slade, Neda / Ciribilli, Yari

    Cancers

    2021  Volume 13, Issue 20

    Abstract: Cutaneous melanoma is the most aggressive form of skin cancer. Despite the significant advances in the management of melanoma in recent decades, it still represents a challenge for clinicians. ... ...

    Abstract Cutaneous melanoma is the most aggressive form of skin cancer. Despite the significant advances in the management of melanoma in recent decades, it still represents a challenge for clinicians. The
    Language English
    Publishing date 2021-10-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers13205231
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Syntheses of gold nanoparticles and their impact on the cell cycle in breast cancer cells subjected to megavoltage X-ray irradiation.

    Hanžić, Nikolina / Horvat, Anđela / Bibić, Juraj / Unfried, Klaus / Jurkin, Tanja / Dražić, Goran / Marijanović, Inga / Slade, Neda / Gotić, Marijan

    Materials science & engineering. C, Materials for biological applications

    2018  Volume 91, Page(s) 486–495

    Abstract: Gold nanoparticles (AuNPs) were synthesized in the presence of citrate (Au-CIT), glutathione (Au-GSH) and aminodextran (Au-DEX) in order to modify AuNPs surfaces and to increase their cellular uptake in the breast cancer cells MDA-MB-231. AuNPs were ... ...

    Abstract Gold nanoparticles (AuNPs) were synthesized in the presence of citrate (Au-CIT), glutathione (Au-GSH) and aminodextran (Au-DEX) in order to modify AuNPs surfaces and to increase their cellular uptake in the breast cancer cells MDA-MB-231. AuNPs were characterized with respect to their particle size, shape and colloidal stability in an aqueous solution and cell media. The mass accumulation of each AuNP type inside cancer cells was determined quantitatively, using Inductive Coupled Plasma - mass spectroscopy. The sub-cellular accumulation was studied using Transmission Electron Microscopy (TEM). It was found that gold nanoparticles applied to cancer cells were localized in cytoplasmic vesicles and that the highest uptake was shown in the presence of Au-GSH nanoparticles. The effect of AuNPs on the cell cycle was investigated using flow cytometry and Western blot analysis. The gold nanoparticles alone did not affect the cell cycle, as shown by flow cytometry. Furthermore, the cancer cells were irradiated using conventional clinically relevant high-energy X-ray radiation of 6 MV in the dose of 4 Gy. The results on cells only irradiated showed an S phase arrest six and 8 h after irradiation, and a G2/M arrest 24 and 48 h after irradiation. The irradiation of breast cancer cells treated with AuNPs has shown no significant variation in cell cycle distribution as opposed to X-ray radiation alone.
    MeSH term(s) Breast Neoplasms/pathology ; Cell Cycle/radiation effects ; Cell Line, Tumor ; Cell Survival/radiation effects ; Endocytosis/drug effects ; Female ; Gold/chemistry ; Humans ; Hydrodynamics ; Metal Nanoparticles/chemistry ; Metal Nanoparticles/ultrastructure ; Spectrophotometry, Ultraviolet ; Subcellular Fractions/metabolism ; X-Rays
    Chemical Substances Gold (7440-57-5)
    Language English
    Publishing date 2018-05-22
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2012160-X
    ISSN 1873-0191 ; 0928-4931
    ISSN (online) 1873-0191
    ISSN 0928-4931
    DOI 10.1016/j.msec.2018.05.066
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Expression profiles of p53/p73, NME and GLI families in metastatic melanoma tissue and cell lines.

    Ozretić, Petar / Hanžić, Nikolina / Proust, Bastien / Sabol, Maja / Trnski, Diana / Radić, Martina / Musani, Vesna / Ciribilli, Yari / Milas, Ivan / Puljiz, Zvonimir / Bosnar, Maja Herak / Levanat, Sonja / Slade, Neda

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 12470

    Abstract: Unlike other tumours, TP53 is rarely mutated in melanoma; however, it fails to function as a tumour suppressor. We assume that its functions might be altered through interactions with several families of proteins, including p53/p73, NME and GLI. To ... ...

    Abstract Unlike other tumours, TP53 is rarely mutated in melanoma; however, it fails to function as a tumour suppressor. We assume that its functions might be altered through interactions with several families of proteins, including p53/p73, NME and GLI. To elucidate the potential interplay among these families we analysed the expression profiles of aforementioned genes and proteins in a panel of melanoma cell lines, metastatic melanoma specimens and healthy corresponding tissue. Using qPCR a higher level of NME1 gene expression and lower levels of Δ40p53β, ΔNp73, GLI1, GLI2 and PTCH1 were observed in tumour samples compared to healthy tissue. Protein expression of Δ133p53α, Δ160p53α and ΔNp73α isoforms, NME1 and NME2, and N'ΔGLI1, GLI1FL, GLI2ΔN isoforms was elevated in tumour tissue, whereas ∆Np73β was downregulated. The results in melanoma cell lines, in general, support these findings. In addition, we correlated expression profiles with clinical features and outcome. Higher Δ133p53β and p53α mRNA and both GLI1 mRNA and GLI3R protein expression had a negative impact on the overall survival. Shorter overall survival was also connected with lower p53β and NME1 gene expression levels. In conclusion, all examined genes may have implications in melanoma development and functional inactivity of TP53.
    MeSH term(s) Cell Line, Tumor ; Disease-Free Survival ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/mortality ; Melanoma/pathology ; Neoplasm Metastasis ; Nucleoside-Diphosphate Kinase/biosynthesis ; Nucleoside-Diphosphate Kinase/genetics ; Survival Rate ; Tumor Protein p73/biosynthesis ; Tumor Protein p73/genetics ; Tumor Suppressor Protein p53/biosynthesis ; Tumor Suppressor Protein p53/genetics
    Chemical Substances TP53 protein, human ; TP73 protein, human ; Tumor Protein p73 ; Tumor Suppressor Protein p53 ; Nucleoside-Diphosphate Kinase (EC 2.7.4.6)
    Language English
    Publishing date 2019-08-28
    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/s41598-019-48882-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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