Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance

Result code in 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>

Alternative codes found

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

Result on the web

<a href="http://apps.webofknowledge.com/InboundService.do?customersID=Alerting&mode=FullRecord&IsProductCode=Yes&product=WOS&Init=Yes&Func=Frame&DestFail=http%3A%2F%2Fwww.webofknowledge.com&action=retrieve&SrcApp=Alerting&SrcAuth=Alerting&SID=C1pXEQmefCtg1cvGeE2&UT=WOS%3A000593509300001" target="_blank" >http://apps.webofknowledge.com/InboundService.do?customersID=Alerting&mode=FullRecord&IsProductCode=Yes&product=WOS&Init=Yes&Func=Frame&DestFail=http%3A%2F%2Fwww.webofknowledge.com&action=retrieve&SrcApp=Alerting&SrcAuth=Alerting&SID=C1pXEQmefCtg1cvGeE2&UT=WOS%3A000593509300001</a>

DOI - Digital Object Identifier

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

Result language

angličtina

Original language name

Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance

Original language description

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.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

30204 - Oncology

Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2020

Confidentiality

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

Name of the periodical

Cancers (Basel)

ISSN

2072-6694

e-ISSN

—

Volume of the periodical

12

Issue of the periodical within the volume

11

Country of publishing house

CH - SWITZERLAND

Number of pages

13

Pages from-to

3227

UT code for WoS article

000593509300001

EID of the result in the Scopus database

2-s2.0-85096573131