Genetic polymorphisms of TLR3 are associated with Nasopharyngeal carcinoma risk in Cantonese population

He, Jiang; Jia, Wei Hua; Fan, Qin; Zhou, Xin Xi; Qin, Hai; Shugart, Yin Yao; Zeng, Yi Xin

doi:10.1186/1471-2407-7-194

Cited by 50 publications

(49 citation statements)

References 41 publications

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“…27 It is proposed that the genetic polymorphisms of TLR3 are associated with nasopharyngeal carcinoma risk. 28 Our data are in line with these previous studies by showing that the exposure to TLR3 ligands, the Poly I:C, activates NPC cells; such an activation induces the expression of miR-21 by NPC cells.…”

Section: Assessment Of the Immune Suppressor Functions Of Npcinduced supporting

confidence: 82%

Nasopharyngeal cancer-derived microRNA-21 promotes immune suppressive B cells

Miao

Zhang

et al. 2014

Cell Mol Immunol

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Section: Assessment Of the Immune Suppressor Functions Of Npcinduced supporting

confidence: 82%

Nasopharyngeal cancer-derived microRNA-21 promotes immune suppressive B cells

Miao

Zhang

et al. 2014

Cell Mol Immunol

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“…Stimulation of TLR3 directly induced cell apoptosis in a poly I:C-dependent manner. nasopharyngeal carcinoma (16). In this study, we clarified that HNSCCs showed varied TLR expression and that they tended to show strong TLR3 expression.…”

Section: Discussionmentioning

confidence: 86%

“…TLR3 is expressed in breast cancer (10), melanoma (11), prostate cancer (12), cervical cancer (13), colon cancer (13), hepatocellular carcinoma (14) and head and neck cancer (15), while TLR4 is expressed in lung cancer (17). In HNSCCs, studies of TLR expression have been reported by only two investigators (15,16). Pries and his colleagues reported TLR3 expression and signaling in HNSCCs (15).…”

Section: Discussionmentioning

confidence: 99%

“…Of the TLRs, TLR3-signaling directly induces apoptosis in a variety of cancer cell lines, including breast cancer, hepatocellular cancer, cervical cancer, colon cancer and melanoma (10)(11)(12)(13)(14). The expression of TLRs and the association of gene polymorphisms of TLR in HNSCC have also been reported (15,16); however, TLR signaling by ligand stimulation in HNSCCs has not yet been closely investigated. In this study, we investigated the expression and signaling of TLRs in HNSCC cell lines, particularly TLR3, and extensively analyzed the proapoptotic activity of TLR3.…”

Section: Introductionmentioning

confidence: 99%

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Toll-like receptor 3 signaling induces apoptosis in human head and neck cancer via survivin associated pathway

Nomi

Kodama²,

Suzuki³

2010

Oncol Rep

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Abstract. The innate immune system builds up host defense against a huge diversity of pathogens, such as viruses, bacteria and fungi. Toll-like receptors (TLRs) are one of the pattern recognition receptors that trigger the initiation of various defense mechanisms. The expression of TLRs represents an important link between innate and adaptive immune responses. The expression of TLRs in several cancer cell types has been reported; however, the exact roles they play in cancers are still unclear. In this study, we investigated the expression and signaling of TLRs in human head and neck squamous cell carcinomas (HNSCCs). The expression of TLRs in 8 HNSCC cell lines was examined by Western blot analysis and flow cytometry. The expression of TLR mRNA was also examined by quantitative RT-PCR. Cells were incubated with poly I:C, a TLR3 ligand, and cell viability was tested by MTT assay. In addition, apoptosis was analyzed by flow cytometry with Annexin V and propidium iodide staining. The expression of survivin, a member of the inhibitors of the apoptosis protein family, was also investigated. TLR2 and TLR3 were widely expressed in human HNSCCs. Interestingly, the stimulation of TLR3 by poly I:C induced apoptosis in cancer cells in a dose-dependent manner. The expression of survivin was down-regulated during apoptosis, suggesting that TLR signaling affects survivinmediated signal transduction in apoptosis. In the present study, we demonstrated the proapoptotic activity of TLR3 expressed by HNSCCs. These results suggest that TLR3 could be a new target for therapy in HNSCCs.

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“…Recently, many studies have investigated the association between TLRs polymorphisms and cancer risk (Zhou et al, 2006;He et al, 2007;Purdue et al, 2009;Ng et al, 2010;Monroy et al, 2011), but the results were inconclusive. Different from the similar meta-analysis in Neoplasma (Wang et al, 2013), the Delta22 polymorphism (-196 to 174 del) was not analyzed in our manuscript.…”

Section: Discussionmentioning

confidence: 99%