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  1. Article ; Online: Cannabinoids in the Modulation of Oxidative Signaling.

    Pagano, Cristina / Savarese, Beatrice / Coppola, Laura / Navarra, Giovanna / Avilia, Giorgio / Laezza, Chiara / Bifulco, Maurizio

    International journal of molecular sciences

    2023  Volume 24, Issue 3

    Abstract: Cannabis sativa-derived compounds, such as delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), and components of the endocannabinoids system, such as N-arachidonoylethanolamide (anandamide, AEA) and 2-arachidonoylglycerol (2-AG), are extensively ... ...

    Abstract Cannabis sativa-derived compounds, such as delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), and components of the endocannabinoids system, such as N-arachidonoylethanolamide (anandamide, AEA) and 2-arachidonoylglycerol (2-AG), are extensively studied to investigate their numerous biological effects, including powerful antioxidant effects. Indeed, a series of recent studies have indicated that many disorders are characterized by alterations in the intracellular antioxidant system, which lead to biological macromolecule damage. These pathological conditions are characterized by an unbalanced, and most often increased, reactive oxygen species (ROS) production. For this study, it was of interest to investigate and recapitulate the antioxidant properties of these natural compounds, for the most part CBD and THC, on the production of ROS and the modulation of the intracellular redox state, with an emphasis on their use in various pathological conditions in which the reduction of ROS can be clinically useful, such as neurodegenerative disorders, inflammatory conditions, autoimmunity, and cancers. The further development of ROS-based fundamental research focused on cannabis sativa-derived compounds could be beneficial for future clinical applications.
    MeSH term(s) Cannabinoids/pharmacology ; Antioxidants ; Reactive Oxygen Species ; Cannabidiol/pharmacology ; Cannabis ; Oxidation-Reduction ; Oxidative Stress ; Dronabinol
    Chemical Substances Cannabinoids ; Antioxidants ; Reactive Oxygen Species ; Cannabidiol (19GBJ60SN5) ; anandamide (UR5G69TJKH) ; Dronabinol (7J8897W37S)
    Language English
    Publishing date 2023-01-28
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24032513
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: N6-isopentenyladenosine inhibits aerobic glycolysis in glioblastoma cells by targeting PKM2 expression and activity.

    Pagano, Cristina / Coppola, Laura / Navarra, Giovanna / Avilia, Giorgio / Savarese, Beatrice / Torelli, Giovanni / Bruzzaniti, Sara / Piemonte, Erica / Galgani, Mario / Laezza, Chiara / Bifulco, Maurizio

    FEBS open bio

    2024  

    Abstract: Glioblastoma (GBM) is a primary tumor in the central nervous system with poor prognosis. It exhibits elevated glucose uptake and lactate production. This metabolic state of aerobic glycolysis is known as the Warburg effect. N6-isopentenyladenosine (iPA), ...

    Abstract Glioblastoma (GBM) is a primary tumor in the central nervous system with poor prognosis. It exhibits elevated glucose uptake and lactate production. This metabolic state of aerobic glycolysis is known as the Warburg effect. N6-isopentenyladenosine (iPA), a natural cytokine modified with an isopentenyl moiety derived from the mevalonate pathway, has well-established anti-tumor activity. It inhibits cell proliferation in glioma cells, inducing cell death by apoptosis and/or necroptosis. In the present study, we found that iPA inhibits aerobic glycolysis in unmodified U87MG cells and in the same cell line engineered to over-express wild-type epidermal growth factor receptor (EGFR) or EGFR variant III (vIII), as well as in a primary GBM4 patient-derived cell line. The detection of glycolysis showed that iPA treatment suppressed ATP and lactate production. We also evaluated the response of iPA treatment in normal human astrocyte primary cells, healthy counterpart cells of the brain. Aerobic glycolysis in treated normal human astrocyte cells did not show significant changes compared to GBM cells. To determine the mechanism of iPA action on aerobic glycolysis, we investigated the expression of certain enzymes involved in this metabolic pathway. We observed that iPA reduced the expression of pyruvate kinase M2 (PKM2), which plays a key role in the regulation of aerobic glycolysis, promoting tumor cell proliferation. The reduction of PKM2 expression is a result of the inhibition of the inhibitor of nuclear factor kappa-B kinase subunit, beta/nuclear factor-kappa B pathway upon iPA treatment. In conclusion, these experimental results show that iPA may inhibit aerobic glycolysis of GBM in stabilized cell lines and primary GBM cells by targeting the expression and activity of PKM2.
    Language English
    Publishing date 2024-03-21
    Publishing country England
    Document type Journal Article
    ZDB-ID 2651702-4
    ISSN 2211-5463 ; 2211-5463
    ISSN (online) 2211-5463
    ISSN 2211-5463
    DOI 10.1002/2211-5463.13766
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Impacts of Environmental Pollution on Brain Tumorigenesis.

    Pagano, Cristina / Navarra, Giovanna / Coppola, Laura / Savarese, Beatrice / Avilia, Giorgio / Giarra, Antonella / Pagano, Giovanni / Marano, Alessandra / Trifuoggi, Marco / Bifulco, Maurizio / Laezza, Chiara

    International journal of molecular sciences

    2023  Volume 24, Issue 5

    Abstract: Pollutants consist of several components, known as direct or indirect mutagens, that can be associated with the risk of tumorigenesis. The increased incidence of brain tumors, observed more frequently in industrialized countries, has generated a deeper ... ...

    Abstract Pollutants consist of several components, known as direct or indirect mutagens, that can be associated with the risk of tumorigenesis. The increased incidence of brain tumors, observed more frequently in industrialized countries, has generated a deeper interest in examining different pollutants that could be found in food, air, or water supply. These compounds, due to their chemical nature, alter the activity of biological molecules naturally found in the body. The bioaccumulation leads to harmful effects for humans, increasing the risk of the onset of several pathologies, including cancer. Environmental components often combine with other risk factors, such as the individual genetic component, which increases the chance of developing cancer. The objective of this review is to discuss the impact of environmental carcinogens on modulating the risk of brain tumorigenesis, focusing our attention on certain categories of pollutants and their sources.
    MeSH term(s) Humans ; Air Pollutants/analysis ; Environmental Pollution ; Air Pollution/analysis ; Environmental Monitoring ; Carcinogenesis ; Brain Neoplasms ; Cell Transformation, Neoplastic ; Brain ; Environmental Exposure
    Chemical Substances Air Pollutants
    Language English
    Publishing date 2023-03-06
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24055045
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Advances in "adiponcosis": Insights in the inner mechanisms at the base of adipose and tumour tissues interplay.

    Pagano, Cristina / di Zazzo, Erika / Avilia, Giorgio / Savarese, Beatrice / Navarra, Giovanna / Proto, Maria Chiara / Fiore, Donatella / Rienzo, Monica / Gazzerro, Patrizia / Laezza, Chiara / Bifulco, Maurizio

    International journal of cancer

    2022  Volume 152, Issue 12, Page(s) 2464–2473

    Abstract: The epidemic spread of obesity is nowadays recognized as a global health and economic burden, arising great interest in the scientific community. The rate of adult obesity steadily increases concomitantly with the cancer incidence. As has been ... ...

    Abstract The epidemic spread of obesity is nowadays recognized as a global health and economic burden, arising great interest in the scientific community. The rate of adult obesity steadily increases concomitantly with the cancer incidence. As has been comprehensively reported, obesity is included among the multiple cancer risk factors and can progressively cause and/or exacerbate certain cancer types, as colorectal and breast cancers. The term adiponcosis was forged precisely to emphasize the interconnection between obesity and cancer onset and progression. The underlying mechanisms of adiponcosis have not been fully elucidated yet, may vary on cancer type, and depend on body fat distribution. It has been proposed that insulin resistance and related chronic hyperinsulinemia, increased insulin-like growth factors production, chronic inflammation or increased bioavailability of steroid hormones could be responsible of cancer hallmarks. Additionally, it has been suggested that adipose tissue-derived hormones, cytokines and adipokines, such as leptin, adiponectin and inflammatory markers, may reflect mechanisms linked to tumorigenesis. This review summarizes the current evidence on pathways, hormones, cytokines and low-chronic inflammation subtending adiponconsis, focusing on breast and colorectal cancers. In addition, we analyzed the lifestyle interventions that could attenuate the driving forces of obesity-related cancer incidence and progression. Moreover, current targets and drugs, their pros and cons, as well as new mechanisms and targets with promising therapeutic potential in cancer are discussed. Depicting this complex interconnection will provide insights for establishing new therapeutic approaches to halt the obesity impacts and thwart cancer onset and progression.
    MeSH term(s) Humans ; Female ; Obesity/complications ; Obesity/metabolism ; Risk Factors ; Breast Neoplasms/metabolism ; Cytokines/metabolism ; Adipose Tissue/metabolism ; Inflammation/complications
    Chemical Substances Cytokines
    Language English
    Publishing date 2022-12-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.34355
    Database MEDical Literature Analysis and Retrieval System OnLINE

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