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.
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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
Original language English
Type of outcome Article in a journal
Field of Study 30204 Oncology
Country of publisher Switzerland
Confidentiality degree is not subject to a state or trade secret
WWW 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
Tags rivok
Tags International impact, Reviewed
Changed by Changed by: Mgr. Marie Šípková, DiS., učo 437722. Changed: 7/1/2021 15:29.
Abstract
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 projectName: Preklinická progrese nových organických sloučenin s cílenou biologickou aktivitou
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