INTERFERON-β FROM MELANOMA CELLS SUPPRESSES THE PROLIFERATIONS OF MELANOMA CELLS IN AN AUTOCRINE MANNER

Satomi, Hisae; Wang, Binghe; Fujisawa, Hiroshi; Otsuka, Fujio

doi:10.1006/cyto.2002.1028

Cited by 32 publications

(22 citation statements)

References 29 publications

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“…The present results add to the growing body of evidence that multiple TLR can induce cell death, as shown for TLR2, TLR4, and TLR5 (4,23,31). With regard to the TLR3-dependent effect on proliferation, a clear cytostatic effect of poly(I:C) on human melanoma cell lines has already been described (32). Although TLR3 involvement was not addressed, it is likely that results from that study are closely related to those described here.…”

Section: Discussionsupporting

confidence: 74%

Toll-like Receptor 3 Expressed by Melanoma Cells as a Target for Therapy?

Salaun

Lebecque

Matikainen

et al. 2007

Clinical Cancer Research

186

145

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Purpose: The immunomodulatory properties of Toll-like receptors (TLR) agonists have inspired their use as experimental adjuvants for vaccination of cancer patients. However, it is now well recognized that TLR expression is not restricted to immune cells but can also be found in many cell types, including those giving rise to tumors. It is therefore mandatory to explore the potential effects of TLR triggering directly on tumor cells. Experimental Design: In the present work, we have investigated TLR3 protein expression in melanoma cell lines derived from patients, and analyzed the effects of TLR3 agonists on tumor cell survival. Moreover, we used RNA interference to stably knock down TLR3 expression and study the involvement of this receptor in dsRNA-induced effects on melanoma cells viability. Results: Human melanoma cells can express functional TLR3 protein. Interestingly, the engagement of the receptor byTLR3 agonists can directly inhibit cell proliferation and induce tumor cell death when combined to treatment with either type I IFN or protein synthesis inhibitors. These effects were shown by RNA interference to be largely dependent on TLR3. Moreover, TLR3-mediated cell death involves the activation of caspases and engages both extrinsic and intrinsic apoptotic pathways. Conclusion: TLR3 protein can be expressed in human melanoma cells, where it can deliver proapoptotic and antiproliferative signaling. Altogether, these results suggest that TLR3 agonists represent very promising adjuvants for cancer vaccines not only based on their well-described immunostimulatory properties, but also due to their newly identified cytostatic and cytotoxic effects directly on tumor cells.

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Section: Discussionsupporting

confidence: 74%

Toll-like Receptor 3 Expressed by Melanoma Cells as a Target for Therapy?

Salaun

Lebecque

Matikainen

et al. 2007

Clinical Cancer Research

186

145

View full text Add to dashboard Cite

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“…Human melanocytes and derived cell lines such as SKMEL-28 can express several inflammatory cytokines such as of IL-1 alpha, IL-1 beta, IL-8, IL-10, IL-12 (p35) and TNF-alpha [4]. Of note, melanocytes will induce the expression of IFN-type I (alpha and beta) particularly in response to single stranded RNA like molecules such as poly I:C to mimic viral infection [5]. However, IFN-beta response of melanocytes is 1000 fold lower when compared to that of human astrocytes or fibroblasts virally-infected [6].…”

Section: Introductionmentioning

confidence: 99%

Regulation of type I-interferon responses in the human epidermal melanocyte cell line SKMEL infected by the Ross River alphavirus

et al. 2015

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“…IFN-␣ is produced by leukocytes and keratinocytes, whereas IFN-␤ is synthesized by a variety of cells (fibroblasts, epithelial cells, and macrophages) [19,20]. Both IFN-␣ and IFNB mRNAs have been detected in normal human melanocytes [21]. IFN-␣ is suggested to be important in enhancing biologic defense activities against oxidative stress [22] and may cause induction of antimelanocyte autoantibodies or activation of cytotoxic T cells [23,24].…”

Section: Introductionmentioning

confidence: 99%