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  1. Article ; Online: NEK6 Regulates Redox Balance and DNA Damage Response in DU-145 Prostate Cancer Cells.

    Pavan, Isadora Carolina Betim / Basei, Fernanda Luisa / Severino, Matheus Brandemarte / Rosa E Silva, Ivan / Issayama, Luidy Kazuo / Mancini, Mariana Camargo Silva / Góis, Mariana Marcela / da Silva, Luiz Guilherme Salvino / Bezerra, Rosangela Maria Neves / Simabuco, Fernando Moreira / Kobarg, Jörg

    Cells

    2023  Volume 12, Issue 2

    Abstract: NEK6 is a central kinase in developing castration-resistant prostate cancer (CRPC). However, the pathways regulated by NEK6 in CRPC are still unclear. Cancer cells have high reactive oxygen species (ROS) levels and easily adapt to this circumstance and ... ...

    Abstract NEK6 is a central kinase in developing castration-resistant prostate cancer (CRPC). However, the pathways regulated by NEK6 in CRPC are still unclear. Cancer cells have high reactive oxygen species (ROS) levels and easily adapt to this circumstance and avoid cell death by increasing antioxidant defenses. We knocked out the NEK6 gene and evaluated the redox state and DNA damage response in DU-145 cells. The knockout of NEK6 decreases the clonogenic capacity, proliferation, cell viability, and mitochondrial activity. Targeting the NEK6 gene increases the level of intracellular ROS; decreases the expression of antioxidant defenses (SOD1, SOD2, and PRDX3); increases JNK phosphorylation, a stress-responsive kinase; and increases DNA damage markers (p-ATM and γH2AX). The exogenous overexpression of NEK6 also increases the expression of these same antioxidant defenses and decreases γH2AX. The depletion of NEK6 also induces cell death by apoptosis and reduces the antiapoptotic Bcl-2 protein. NEK6-lacking cells have more sensitivity to cisplatin. Additionally, NEK6 regulates the nuclear localization of NF-κB2, suggesting NEK6 may regulate NF-κB2 activity. Therefore, NEK6 alters the redox balance, regulates the expression of antioxidant proteins and DNA damage, and its absence induces the death of DU-145 cells. NEK6 inhibition may be a new strategy for CRPC therapy.
    MeSH term(s) Male ; Humans ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Reactive Oxygen Species/metabolism ; Cell Line, Tumor ; Antioxidants/metabolism ; NF-kappa B p52 Subunit/metabolism ; Oxidation-Reduction ; DNA Damage ; NIMA-Related Kinases/genetics ; NIMA-Related Kinases/metabolism
    Chemical Substances Reactive Oxygen Species ; Antioxidants ; NF-kappa B p52 Subunit ; NEK6 protein, human (EC 2.7.11.1) ; NIMA-Related Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2023-01-07
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12020256
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The Hallmarks of Flavonoids in Cancer.

    Ponte, Luis Gustavo Saboia / Pavan, Isadora Carolina Betim / Mancini, Mariana Camargo Silva / da Silva, Luiz Guilherme Salvino / Morelli, Ana Paula / Severino, Matheus Brandemarte / Bezerra, Rosangela Maria Neves / Simabuco, Fernando Moreira

    Molecules (Basel, Switzerland)

    2021  Volume 26, Issue 7

    Abstract: Flavonoids represent an important group of bioactive compounds derived from plant-based foods and beverages with known biological activity in cells. From the modulation of inflammation to the inhibition of cell proliferation, flavonoids have been ... ...

    Abstract Flavonoids represent an important group of bioactive compounds derived from plant-based foods and beverages with known biological activity in cells. From the modulation of inflammation to the inhibition of cell proliferation, flavonoids have been described as important therapeutic adjuvants against several diseases, including diabetes, arteriosclerosis, neurological disorders, and cancer. Cancer is a complex and multifactor disease that has been studied for years however, its prevention is still one of the best known and efficient factors impacting the epidemiology of the disease. In the molecular and cellular context, some of the mechanisms underlying the oncogenesis and the progression of the disease are understood, known as the hallmarks of cancer. In this text, we review important molecular signaling pathways, including inflammation, immunity, redox metabolism, cell growth, autophagy, apoptosis, and cell cycle, and analyze the known mechanisms of action of flavonoids in cancer. The current literature provides enough evidence supporting that flavonoids may be important adjuvants in cancer therapy, highlighting the importance of healthy and balanced diets to prevent the onset and progression of the disease.
    MeSH term(s) Animals ; Clinical Trials as Topic ; Flavonoids/administration & dosage ; Flavonoids/chemistry ; Flavonoids/pharmacology ; Flavonoids/therapeutic use ; Humans ; Immunity/drug effects ; Inflammation/pathology ; Neoplasms/drug therapy ; Neoplasms/immunology ; Signal Transduction/drug effects
    Chemical Substances Flavonoids
    Language English
    Publishing date 2021-04-02
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1413402-0
    ISSN 1420-3049 ; 1431-5165 ; 1420-3049
    ISSN (online) 1420-3049
    ISSN 1431-5165 ; 1420-3049
    DOI 10.3390/molecules26072029
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.MO 81: Show issues

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  3. Article ; Online: Effects of short-term endurance and strength exercise in the molecular regulation of skeletal muscle in hyperinsulinemic and hyperglycemic Slc2a4

    Muñoz, Vitor Rosetto / Botezelli, José Diego / Gaspar, Rafael Calais / da Rocha, Alisson L / Vieira, Renan Fudoli Lins / Crisol, Barbara Moreira / Braga, Renata Rosseto / Severino, Matheus Brandemarte / Nakandakari, Susana Castelo Branco Ramos / Antunes, Gabriel Calheiros / Brunetto, Sérgio Q / Ramos, Celso D / Velloso, Lício Augusto / Simabuco, Fernando Moreira / de Moura, Leandro Pereira / da Silva, Adelino Sanchez Ramos / Ropelle, Eduardo Rochete / Cintra, Dennys Esper / Pauli, José Rodrigo

    Cellular and molecular life sciences : CMLS

    2023  Volume 80, Issue 5, Page(s) 122

    Abstract: Objective: Intriguingly, hyperinsulinemia, and hyperglycemia can predispose insulin resistance, obesity, and type 2 diabetes, leading to metabolic disturbances. Conversely, physical exercise stimulates skeletal muscle glucose uptake, improving whole- ... ...

    Abstract Objective: Intriguingly, hyperinsulinemia, and hyperglycemia can predispose insulin resistance, obesity, and type 2 diabetes, leading to metabolic disturbances. Conversely, physical exercise stimulates skeletal muscle glucose uptake, improving whole-body glucose homeostasis. Therefore, we investigated the impact of short-term physical activity in a mouse model (Slc2a4
    Methods: Slc2a4
    Results: When Slc2a4
    Conclusions: Both short-term exercise protocols were efficient in whole-body glucose homeostasis and insulin resistance. While endurance exercise plays an important role in transcriptome and mitochondrial activity, strength exercise mostly affects post-translational mechanisms and protein synthesis in skeletal muscle. Thus, the performance of both types of physical exercise proved to be a very effective way to mitigate the impacts of hyperglycemia and hyperinsulinemia in the Slc2a4
    MeSH term(s) Mice ; Animals ; Insulin Resistance ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Muscle, Skeletal/metabolism ; Hyperglycemia/genetics ; Hyperglycemia/metabolism ; Glucose/metabolism ; Glucose Transporter Type 4/metabolism
    Chemical Substances Glucose (IY9XDZ35W2) ; Slc2a4 protein, mouse ; Glucose Transporter Type 4
    Language English
    Publishing date 2023-04-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-023-04771-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 195: 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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  4. Article ; Online: Characterization of the Interaction Between SARS-CoV-2 Membrane Protein (M) and Proliferating Cell Nuclear Antigen (PCNA) as a Potential Therapeutic Target.

    Zambalde, Érika Pereira / Pavan, Isadora Carolina Betim / Mancini, Mariana Camargo Silva / Severino, Matheus Brandemarte / Scudero, Orlando Bonito / Morelli, Ana Paula / Amorim, Mariene Ribeiro / Bispo-Dos-Santos, Karina / Góis, Mariana Marcela / Toledo-Teixeira, Daniel A / Parise, Pierina Lorencini / Mauad, Thais / Dolhnikoff, Marisa / Saldiva, Paulo Hilário Nascimento / Marques-Souza, Henrique / Proenca-Modena, José Luiz / Ventura, Armando Morais / Simabuco, Fernando Moreira

    Frontiers in cellular and infection microbiology

    2022  Volume 12, Page(s) 849017

    Abstract: SARS-CoV-2 is an emerging virus from the Coronaviridae family and is responsible for the ongoing COVID-19 pandemic. In this work, we explored the previously reported SARS-CoV-2 structural membrane protein (M) interaction with human Proliferating Cell ... ...

    Abstract SARS-CoV-2 is an emerging virus from the Coronaviridae family and is responsible for the ongoing COVID-19 pandemic. In this work, we explored the previously reported SARS-CoV-2 structural membrane protein (M) interaction with human Proliferating Cell Nuclear Antigen (PCNA). The M protein is responsible for maintaining virion shape, and PCNA is a marker of DNA damage which is essential for DNA replication and repair. We validated the M-PCNA interaction through immunoprecipitation, immunofluorescence co-localization, and PLA (Proximity Ligation Assay). In cells infected with SARS-CoV-2 or transfected with M protein, using immunofluorescence and cell fractioning, we documented a reallocation of PCNA from the nucleus to the cytoplasm and the increase of PCNA and γH2AX (another DNA damage marker) expression. We also observed an increase in PCNA and γH2AX expression in the lung of a COVID-19 patient by immunohistochemistry. In addition, the inhibition of PCNA translocation by PCNA I1 and Verdinexor led to a reduction of plaque formation in an
    MeSH term(s) Coronavirus M Proteins/metabolism ; Humans ; Proliferating Cell Nuclear Antigen/metabolism ; SARS-CoV-2 ; COVID-19 Drug Treatment
    Chemical Substances Coronavirus M Proteins ; PCNA protein, human ; Proliferating Cell Nuclear Antigen ; membrane protein, SARS-CoV-2
    Language English
    Publishing date 2022-05-23
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2619676-1
    ISSN 2235-2988 ; 2235-2988
    ISSN (online) 2235-2988
    ISSN 2235-2988
    DOI 10.3389/fcimb.2022.849017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: STAT3 contributes to cisplatin resistance, modulating EMT markers, and the mTOR signaling in lung adenocarcinoma.

    Morelli, Ana Paula / Tortelli, Tharcísio Citrângulo / Mancini, Mariana Camargo Silva / Pavan, Isadora Carolina Betim / Silva, Luiz Guilherme Salvino / Severino, Matheus Brandemarte / Granato, Daniela Campos / Pestana, Nathalie Fortes / Ponte, Luis Gustavo Saboia / Peruca, Guilherme Francisco / Pauletti, Bianca Alves / Dos Santos, Daniel Francisco Guimarães / de Moura, Leandro Pereira / Bezerra, Rosângela Maria Neves / Leme, Adriana Franco Paes / Chammas, Roger / Simabuco, Fernando Moreira

    Neoplasia (New York, N.Y.)

    2021  Volume 23, Issue 10, Page(s) 1048–1058

    Abstract: Lung cancer is the second leading cause of cancer death worldwide and is strongly associated with cisplatin resistance. The transcription factor signal transducer and activator of transcription 3 (STAT3) is constitutively activated in cancer cells and ... ...

    Abstract Lung cancer is the second leading cause of cancer death worldwide and is strongly associated with cisplatin resistance. The transcription factor signal transducer and activator of transcription 3 (STAT3) is constitutively activated in cancer cells and coordinates critical cellular processes as survival, self-renewal, and inflammation. In several types of cancer, STAT3 controls the development, immunogenicity, and malignant behavior of tumor cells while it dictates the responsiveness to radio- and chemotherapy. It is known that STAT3 phosphorylation at Ser727 by mechanistic target of rapamycin (mTOR) is necessary for its maximal activation, but the crosstalk between STAT3 and mTOR signaling in cisplatin resistance remains elusive. In this study, using a proteomic approach, we revealed important targets and signaling pathways altered in cisplatin-resistant A549 lung adenocarcinoma cells. STAT3 had increased expression in a resistance context, which can be associated with a poor prognosis. STAT3 knockout (SKO) resulted in a decreased mesenchymal phenotype in A549 cells, observed by clonogenic potential and by the expression of epithelial-mesenchymal transition markers. Importantly, SKO cells did not acquire the mTOR pathway overactivation induced by cisplatin resistance. Consistently, SKO cells were more responsive to mTOR inhibition by rapamycin and presented impairment of the feedback activation loop in Akt. Therefore, rapamycin was even more potent in inhibiting the clonogenic potential in SKO cells and sensitized to cisplatin treatment. Mechanistically, STAT3 partially coordinated the cisplatin resistance phenotype via the mTOR pathway in non-small cell lung cancer. Thus, our findings reveal important targets and highlight the significance of the crosstalk between STAT3 and mTOR signaling in cisplatin resistance. The synergic inhibition of STAT3 and mTOR potentially unveil a potential mechanism of synthetic lethality to be explored for human lung cancer treatment.
    Language English
    Publishing date 2021-09-17
    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.2021.08.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5203: 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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