TLR4 in skin cancer: From molecular mechanisms to clinical interventions

Dickinson, Sally E.; Wondrak, Georg T.

doi:10.1002/mc.23016

Cited by 20 publications

(17 citation statements)

References 78 publications

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“…Sequence pairing analysis showed that lncRNA H19 and TLR4 shared common binding loci on the miR-17 sequence, and DLR assay confirmed that lncRNA H19 and TLR4 could bind to TLR4 is an important member of cellular immunity and mediates the release of proinflammatory factors, 26 and its abnormal expression may trigger a series of diseases or cancers. [27][28][29][30] In the case of adenomyosis, the inflammatory response induced by TLR4 promotes the excessive proliferation of ESCs and endows them with invasive phenotypes, 31 resulting in the cells to invade to myometrium. According to our findings, LVG reduces the level of TLR4 in ESCs by regulating lncRNA H19/miR-17, thus attenuating the inflammatory response (down-regulation of TNF-α, IL-6, IL-8, IL-17 and IL-1β), and finally suppressing the excessive proliferation and malignant proliferation of ESCs.…”

Section: Discussionmentioning

confidence: 99%

<p>Levonorgestrel Ameliorates Adenomyosis via lncRNA H19/miR-17/TLR4 Pathway</p>

Liang¹,

Zhang²,

Wang³

et al. 2020

DDDT

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To explore the mechanism of levonorgestrel (LNG)-ameliorating adenomyosis through long non-coding RNA H19 (lncRNA H19)/miR-17/Toll-like receptor 4 (TLR4) pathway. Patients and Methods: A total of 71 cases of adenomyosis and 54 cases of normal endometrium were sampled. Quantitative polymerase chain reaction (qPCR) was employed to quantify lncRNA H19, miR-17, and TLR4 mRNA, while Western blot (WB) was used to quantify TLR4 protein. Effects of LNG on normal endometrial stromal cells (ESCs) were evaluated. Suppression/over-expression vectors of lncRNA H19, miR-17, and TLR4 were constructed to observe their effects on ESCs. Results: MiR-17 and TLR4 mRNA were up-regulated and lncRNA H19 was downregulated in adenomyosis. After LNG treatment, lncRNA H19 was up-regulated while miR-17 and TLR4 were down-regulated. LNG, up-regulation of lncRNA H19, and downregulation of miR-17 and TLR4 portend increased apoptosis, G1-arrested cells, as well as inhibited inflammation. Dual-luciferase reporter (DLR) assay conformed the targeting relation of lncRNA H19/miR-17/TLR4 pathway. Conclusion: LNG ameliorates adenomyosis via lncRNA H19/miR-17/TLR4 pathway.

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Section: Discussionmentioning

confidence: 99%

<p>Levonorgestrel Ameliorates Adenomyosis via lncRNA H19/miR-17/TLR4 Pathway</p>

Liang¹,

Zhang²,

Wang³

et al. 2020

DDDT

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“…Among various TLRs, TLR4 is known to play a pivotal role in both skin inflammation and cancer. Activation of TLR4 and subsequent internal signaling pathways can induce the activation of transcription factors including NF-κB, IRF-3, and AP-1, which affect the expression of genes associated with inflammation, cellular apoptosis, survival, and differentiation [72]. As a matter of fact, increased expression of TLRs has been observed in skin cancers.…”

Section: The Skin Immune System and Skin Cancermentioning

confidence: 99%

The Human Microbiota and Skin Cancer

Woo

Cho

Lee

et al. 2022

IJMS

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Skin cancer is the most common type of cancer in the US with an increasing prevalence worldwide. While ultraviolet (UV) radiation is a well-known risk factor, there is emerging evidence that the microbiota may also contribute. In recent years, the human microbiota has become a topic of great interest, and its association with inflammatory skin diseases (i.e., atopic dermatitis, acne, rosacea) has been explored. Little is known of the role of microbiota in skin cancer, but with the recognized link between microbial dysbiosis and inflammation, and knowledge that microbiota modulates the effect of UV-induced immunosuppression, theories connecting the two have surfaced. In this paper, we provide a comprehensive review of the key literature on human microbiota, especially the skin microbiota, and skin cancer (i.e., non-melanoma skin cancer, melanoma, cutaneous T cell lymphoma). Also, mechanistic perspectives as to how our microbiota influence skin cancer development and treatment are offered.

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“…TLRs respond to acute inflammatory signals either from microbial sources (PAMPs, pathogen-associated molecular patterns) or selfderived stress signals (DAMPs), the role that also hyaluronan has been proposed to play. The activation of TLR signaling leads to NF-kB, AP-1 and/or IRF-3 mediated inflammatory response in healthy skin and in primary melanocytes and eventually skin carcinogenesis (94,127). This suggests a role for hyaluronan metabolism, especially for UV-induced hyaluronan fragmentation via TLR4-mediated inflammation, in melanocyte transformation process towards cutaneous melanoma.…”

Section: Hyaluronan In Inflammatory Reactionsmentioning

confidence: 99%

The Impact of Hyaluronan on Tumor Progression in Cutaneous Melanoma

et al. 2022

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The incidence of cutaneous melanoma is rapidly increasing worldwide. Cutaneous melanoma is an aggressive type of skin cancer, which originates from malignant transformation of pigment producing melanocytes. The main risk factor for melanoma is ultraviolet (UV) radiation, and thus it often arises from highly sun-exposed skin areas and is characterized by a high mutational burden. In addition to melanoma-associated mutations such as BRAF, NRAS, PTEN and cell cycle regulators, the expansion of melanoma is affected by the extracellular matrix surrounding the tumor together with immune cells. In the early phases of the disease, hyaluronan is the major matrix component in cutaneous melanoma microenvironment. It is a high-molecular weight polysaccharide involved in several physiological and pathological processes. Hyaluronan is involved in the inflammatory reactions associated with UV radiation but its role in melanomagenesis is still unclear. Although abundant hyaluronan surrounds epidermal and dermal cells in normal skin and benign nevi, its content is further elevated in dysplastic lesions and local tumors. At this stage hyaluronan matrix may act as a protective barrier against melanoma progression, or alternatively against immune cell attack. While in advanced melanoma, the content of hyaluronan decreases due to altered synthesis and degradation, and this correlates with poor prognosis. This review focuses on hyaluronan matrix in cutaneous melanoma and how the changes in hyaluronan metabolism affect the progression of melanoma.

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TLR4 in skin cancer: From molecular mechanisms to clinical interventions

Cited by 20 publications

References 78 publications

<p>Levonorgestrel Ameliorates Adenomyosis via lncRNA H19/miR-17/TLR4 Pathway</p>

<p>Levonorgestrel Ameliorates Adenomyosis via lncRNA H19/miR-17/TLR4 Pathway</p>

The Human Microbiota and Skin Cancer

The Impact of Hyaluronan on Tumor Progression in Cutaneous Melanoma

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