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

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About: Blocking drug-induced autophagy with chloroquine in HCT-116 colon cancer cells enhances DC maturation and T cell responses induced by tumor cell lysate Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Blocking drug-induced autophagy with chloroquine in HCT-116 colon cancer cells enhances DC maturation and T cell responses induced by tumor cell lysate
Creator	Lotze, Michael Santos, Pessoa, João Andree, Jofer Carvalho, Daniela Falasco, Bianca Fogolin, Carla Gorgulho, Carolina Junior, Araújo Kaneno, Ramon Portes Ureshino, Rodrigo Ramirez, Zamame Romagnoli, Graziela
Source	Elsevier; Medline; PMC
abstract	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.
has issue date	2020-07-31(xsd:dateTime)
bibo:doi	10.1016/j.intimp.2020.106495
bibo:pmid	32298965
has license	els-covid
sha1sum (hex)	cd2f584c21a2bc13a089348c021044609e55dc06
schema:url	https://doi.org/10.1016/j.intimp.2020.106495
resource representing a document's title	Blocking drug-induced autophagy with chloroquine in HCT-116 colon cancer cells enhances DC maturation and T cell responses induced by tumor cell lysate
has PubMed Central identifier	PMC7152898
has PubMed identifier	32298965
schema:publication	International Immunopharmacology
resource representing a document's body	covid:cd2f584c21a2bc13a089348c021044609e55dc06#body_text
is schema:about of	named entity 'damage' named entity 'stimulate' named entity 'higher' named entity 'expression' named entity 'genes' named entity 'expanded' named entity '5-FLUOROURACIL' named entity 'HCT-116 CELLS' named entity 'MECHANISM' named entity 'DEVELOPMENT' named entity 'CD4' named entity 'IMPROVED' named entity 'EXPRESSION' named entity 'PD-1' named entity 'HIGHER' named entity 'FAMILY' named entity 'RADIATION THERAPY' named entity 'LOWER' named entity 'BNIP3L' named entity 'AGENT' named entity 'T CELL' named entity 'THEIR' named entity 'T CELLS' named entity 'tumor progression' named entity 'cells' named entity 'CD107a' named entity 'efficacy' named entity 'lysate' named entity 'resistance' named entity 'recover' named entity 'dendritic cell' named entity 'DCs' named entity 'maturation' named entity 'maturation' named entity 'select' named entity 'combination' named entity 'chloroquine' named entity 'T cells' named entity 'greater' named entity 'expression of genes' named entity 'tumor' named entity 'chemotherapy' named entity 'antineoplastic agents' named entity 'BNIP3L' named entity 'DCs' named entity 'DCs' named entity 'pharmacological' named entity 'IFN-γ' named entity 'HES1' named entity 'LOXL2' named entity 'DCs' named entity 'autophagy' named entity 'tumor suppressors' named entity 'expression of genes' named entity 'colon cancer cells' named entity 'cell lysate' named entity 'autophagy' named entity 'T cell' named entity 'HCT-116' named entity '5-FU' named entity 'HCT-116' named entity 'lysate' named entity 'DCs' named entity 'Biotechnology' named entity 'lysates' named entity 'western blot' named entity 'high mobility group' named entity '5-FU' named entity 'vesicles'

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