Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance

J 2020

Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance

MURESAN, Ximena Maria, Jan BOUCHAL, Zoran CULIG and Karel SOUČEK

Basic information

Original name

Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance

Authors

MURESAN, Ximena Maria, Jan BOUCHAL, Zoran CULIG and Karel SOUČEK (203 Czech Republic, guarantor, belonging to the institution)

Edition

Cancers, Basel, MDPI, 2020, 2072-6694

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

30204 Oncology

Country of publisher

Switzerland

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

URL

Impact factor

Impact factor: 6.639

RIV identification code

RIV/00216224:14310/20:00117618

Organization unit

Faculty of Science

DOI

http://dx.doi.org/10.3390/cancers12113227

UT WoS

000593509300001

Keywords in English

toll-like receptor 3; therapy resistance; cytokines; dsRNA; metastasis

Abstract

V originále

Toll-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.

Links

EF16_025/0007381, research and development project

Name: Preklinická progrese nových organických sloučenin s cílenou biologickou aktivitou

Citovat

MURESAN, Ximena Maria, Jan BOUCHAL, Zoran CULIG and Karel SOUČEK. Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance. Cancers. Basel: MDPI, 2020, vol. 12, No 11, p. 1-13. ISSN 2072-6694. Available from: https://dx.doi.org/10.3390/cancers12113227.

@article{1721737,
   author = {Muresan, Ximena Maria and Bouchal, Jan and Culig, Zoran and Souček, Karel},
   article_location = {Basel},
   article_number = {11},
   doi = {http://dx.doi.org/10.3390/cancers12113227},
   keywords = {toll-like receptor 3; therapy resistance; cytokines; dsRNA; metastasis},
   language = {eng},
   issn = {2072-6694},
   journal = {Cancers},
   title = {Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance},
   url = {https://doi.org/10.3390/cancers12113227},
   volume = {12},
   year = {2020}
}

TY  - JOUR
ID  - 1721737
AU  - Muresan, Ximena Maria - Bouchal, Jan - Culig, Zoran - Souček, Karel
PY  - 2020
TI  - Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance
JF  - Cancers
VL  - 12
IS  - 11
SP  - 1-13
EP  - 1-13
PB  - MDPI
SN  - 20726694
KW  - toll-like receptor 3
KW  - therapy resistance
KW  - cytokines
KW  - dsRNA
KW  - metastasis
UR  - https://doi.org/10.3390/cancers12113227
L2  - https://doi.org/10.3390/cancers12113227
N2  - Toll-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.
ER  -

MURESAN, Ximena Maria, Jan BOUCHAL, Zoran CULIG and Karel SOUČEK. Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance. \textit{Cancers}. Basel: MDPI, 2020, vol.~12, No~11, p.~1-13. ISSN~2072-6694. Available from: https://dx.doi.org/10.3390/cancers12113227.

Detailed Information on Publication Record