Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F20%3A00536528" target="_blank" >RIV/68081707:_____/20:00536528 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00159816:_____/20:00073509 RIV/00216224:14310/20:00117618 RIV/61989592:15110/20:73602662

Výsledek na webu

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DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/cancers12113227" target="_blank" >10.3390/cancers12113227</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance

Popis výsledku v původním jazyce

Simple SummarynToll-like receptor 3 (TLR3) is a member of the TLR family, which has been extensively studied for the antiviral function and, therefore, its role in the innate and adaptive immune responses. It is highly expressed in the endosomes of antigen-presenting immune cells and epithelial cells. Several studies have demonstrated TLR3 expression in multiple neoplasia types including breast, prostate, and ovarian cancer. In this perspective, we focus on the mechanisms through which TLR3 can either lead to tumor regression or promote carcinogenesis as well as on the potential of TLR-based therapies in resistant cancer.nnToll-like receptor 3 (TLR3) is a member of the TLR family, which has been extensively studied for its antiviral function. It is highly expressed in the endosomes of antigen-presenting immune cells and epithelial cells. TLR3 binds specifically double-strand RNAs (dsRNAs), leading to the activation of mainly two downstream pathways: the phosphorylation of IRF3, with subsequent production of type I interferon, and the activation of NF-kappa B, which drives the production of inflammatory cytokines and chemokines. Several studies have demonstrated TLR3 expression in multiple neoplasia types including breast, prostate, and lung cancer. Most studies were focused on the beneficial role of TLR3 activation in tumor cells, which leads to the production of cytotoxic cytokines and interferons and promotes caspase-dependent apoptosis. Indeed, ligands of this receptor were proposed for the treatment of cancer, also in combination with conventional chemotherapy. In contrast to these findings, recent evidence showed a link between TLR3 and tumor progression, metastasis, and therapy resistance. In the present review, we summarize the current knowledge of the mechanisms through which TLR3 can either lead to tumor regression or promote carcinogenesis as well as the potential of TLR-based therapies in resistant cancer.

Název v anglickém jazyce

Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance

Popis výsledku anglicky

Simple SummarynToll-like receptor 3 (TLR3) is a member of the TLR family, which has been extensively studied for the antiviral function and, therefore, its role in the innate and adaptive immune responses. It is highly expressed in the endosomes of antigen-presenting immune cells and epithelial cells. Several studies have demonstrated TLR3 expression in multiple neoplasia types including breast, prostate, and ovarian cancer. In this perspective, we focus on the mechanisms through which TLR3 can either lead to tumor regression or promote carcinogenesis as well as on the potential of TLR-based therapies in resistant cancer.nnToll-like receptor 3 (TLR3) is a member of the TLR family, which has been extensively studied for its antiviral function. It is highly expressed in the endosomes of antigen-presenting immune cells and epithelial cells. TLR3 binds specifically double-strand RNAs (dsRNAs), leading to the activation of mainly two downstream pathways: the phosphorylation of IRF3, with subsequent production of type I interferon, and the activation of NF-kappa B, which drives the production of inflammatory cytokines and chemokines. Several studies have demonstrated TLR3 expression in multiple neoplasia types including breast, prostate, and lung cancer. Most studies were focused on the beneficial role of TLR3 activation in tumor cells, which leads to the production of cytotoxic cytokines and interferons and promotes caspase-dependent apoptosis. Indeed, ligands of this receptor were proposed for the treatment of cancer, also in combination with conventional chemotherapy. In contrast to these findings, recent evidence showed a link between TLR3 and tumor progression, metastasis, and therapy resistance. In the present review, we summarize the current knowledge of the mechanisms through which TLR3 can either lead to tumor regression or promote carcinogenesis as well as the potential of TLR-based therapies in resistant cancer.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30204 - Oncology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2020

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Cancers (Basel)

ISSN

2072-6694

e-ISSN

—

Svazek periodika

12

Číslo periodika v rámci svazku

11

Stát vydavatele periodika

CH - Švýcarská konfederace

Počet stran výsledku

13

Strana od-do

3227

Kód UT WoS článku

000593509300001

EID výsledku v databázi Scopus

2-s2.0-85096573131