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  1. Article ; Online: Inhibiting autophagy to prevent drug resistance and improve anti-tumor therapy.

    Zamame Ramirez, Jofer Andree / Romagnoli, Graziela Gorete / Kaneno, Ramon

    Life sciences

    2020  Volume 265, Page(s) 118745

    Abstract: Cytotoxic drugs remain the first-line option for cancer therapy but the development of drug-resistance by tumor cells represents a primary obstacle for successful chemotherapy. Autophagy is a physiological mechanism of cell survival efficiently used by ... ...

    Abstract Cytotoxic drugs remain the first-line option for cancer therapy but the development of drug-resistance by tumor cells represents a primary obstacle for successful chemotherapy. Autophagy is a physiological mechanism of cell survival efficiently used by tumor cells to avoid cell death and to induce drug-resistance. It is a macromolecular process, in which cells degrade and recycle intracellular substrates and damaged organelles to alleviate cell stress caused by nutritional deprivation, hypoxia, irradiation, and cytotoxic agents, as well. There is evidence that autophagy prevents cancer during the early steps of carcinogenesis, but once transformed, these cells show enhanced autophagy capacity and use it to survive, grow, and facilitate metastasis. Current basic studies and clinical trials show the feasibility of using pharmacological or molecular blockage of autophagy to improve the anticancer therapy efficiency. In this review, we overviewed the pathways and molecular aspects of autophagy, its role in carcinogenesis, and the evidence for its role in cancer adaptation and drug-resistance. Finally, we reviewed the clinical findings on how the autophagy interference helps to improve conventional anticancer therapy.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Autophagy/drug effects ; Autophagy/physiology ; Cell Death/drug effects ; Cell Survival/drug effects ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Drug Resistance, Neoplasm/physiology ; Humans ; Neoplasms/drug therapy ; Signal Transduction/drug effects
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2020-11-10
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2020.118745
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.368: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  2. Article: Inhibiting autophagy to prevent drug resistance and improve anti-tumor therapy

    Zamame Ramirez, Jofer Andree / Romagnoli, Graziela Gorete / Kaneno, Ramon

    Life sciences. 2021 Jan. 15, v. 265

    2021  

    Abstract: Cytotoxic drugs remain the first-line option for cancer therapy but the development of drug-resistance by tumor cells represents a primary obstacle for successful chemotherapy. Autophagy is a physiological mechanism of cell survival efficiently used by ... ...

    Abstract Cytotoxic drugs remain the first-line option for cancer therapy but the development of drug-resistance by tumor cells represents a primary obstacle for successful chemotherapy. Autophagy is a physiological mechanism of cell survival efficiently used by tumor cells to avoid cell death and to induce drug-resistance. It is a macromolecular process, in which cells degrade and recycle intracellular substrates and damaged organelles to alleviate cell stress caused by nutritional deprivation, hypoxia, irradiation, and cytotoxic agents, as well. There is evidence that autophagy prevents cancer during the early steps of carcinogenesis, but once transformed, these cells show enhanced autophagy capacity and use it to survive, grow, and facilitate metastasis. Current basic studies and clinical trials show the feasibility of using pharmacological or molecular blockage of autophagy to improve the anticancer therapy efficiency. In this review, we overviewed the pathways and molecular aspects of autophagy, its role in carcinogenesis, and the evidence for its role in cancer adaptation and drug-resistance. Finally, we reviewed the clinical findings on how the autophagy interference helps to improve conventional anticancer therapy.
    Keywords autophagy ; cancer therapy ; carcinogenesis ; cell viability ; cytotoxicity ; drug resistance ; drug therapy ; hypoxia ; irradiation ; metastasis ; neoplasms ; organelles
    Language English
    Dates of publication 2021-0115
    Publishing place Elsevier Inc.
    Document type Article
    Note NAL-light
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2020.118745
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

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  3. Article ; Online: Blocking drug-induced autophagy with chloroquine in HCT-116 colon cancer cells enhances DC maturation and T cell responses induced by tumor cell lysate.

    Zamame Ramirez, Jofer Andree / Romagnoli, Graziela Gorete / Falasco, Bianca Francisco / Gorgulho, Carolina Mendonça / Sanzochi Fogolin, Carla / Dos Santos, Daniela Carvalho / Junior, João Pessoa Araújo / Lotze, Michael Thomas / Ureshino, Rodrigo Portes / Kaneno, Ramon

    International immunopharmacology

    2020  Volume 84, Page(s) 106495

    Abstract: Autophagy is an important mechanism for tumor escape, allowing tumor cells to recover from the damage induced by chemotherapy, radiation therapy, and immunotherapy and contributing to the development of resistance. The pharmacological inhibition of ... ...

    Abstract Autophagy is an important mechanism for tumor escape, allowing tumor cells to recover from the damage induced by chemotherapy, radiation therapy, and immunotherapy and contributing to the development of resistance. The pharmacological inhibition of autophagy contributes to increase the efficacy of antineoplastic agents. Exposing tumor cells to low concentrations of select autophagy-inducing antineoplastic agents increases their immunogenicity and enhances their ability to stimulate dendritic cell (DC) maturation. We tested whether the application of an autophagy-inhibiting agent, chloroquine (CQ), in combination with low concentrations of 5-fluorouracil (5-FU) increases the ability of tumor cells to induce DC maturation. DCs sensitized with the lysate of HCT-116 cells previously exposed to such a combination enhanced the DC maturation/activation ability. These matured DCs also increased the allogeneic responsiveness of both CD4+ and CD8+ T cells, which showed a greater proliferative response than those from DCs sensitized with control lysates. The T cells expanded in such cocultures were CD69+ and PD-1- and produced higher levels of IFN-γ and lower levels of IL-10, consistent with the preferential activation of Th1 cells. Cocultures of autologous DCs and lymphocytes improved the generation of cytotoxic T lymphocytes, as assessed by the expression of CD107a, perforin, and granzyme B. The drug combination increased the expression of genes related to the CEACAM family (BECN1, ATGs, MAPLC3B, ULK1, SQSTM1) and tumor suppressors (PCBP1). Furthermore, the decreased expression of genes related to metastasis and tumor progression (BNIP3, BNIP3L, FOSL2, HES1, LAMB3, LOXL2, NDRG1, P4HA1, PIK3R2) was noted. The combination of 5-FU and CQ increases the ability of tumor cells to drive DC maturation and enhances the ability of DCs to stimulate T cell responses.
    MeSH term(s) Antimetabolites, Antineoplastic/pharmacology ; Autophagy/drug effects ; CD4-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/metabolism ; Cell Differentiation/drug effects ; Chloroquine/pharmacology ; Dendritic Cells/cytology ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Fluorouracil/pharmacology ; HCT116 Cells ; Humans ; Lymphocyte Activation/drug effects ; Th1 Cells/drug effects ; Th1 Cells/metabolism ; Transcriptional Activation/drug effects
    Chemical Substances Antimetabolites, Antineoplastic ; Chloroquine (886U3H6UFF) ; Fluorouracil (U3P01618RT)
    Keywords covid19
    Language English
    Publishing date 2020-04-13
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2020.106495
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5408: 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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