INDUCTION OF PROINFLAMMATORY AND CHEMOKINE GENES BY LIPOPOLYSACCHARIDE AND PACLITAXEL (Taxol™) IN MURINE AND HUMAN BREAST CANCER CELL LINES

Zaks-Zilberman, Meirav; Zaks, Tal; Vogel, Stefanie N.

doi:10.1006/cyto.2001.0935

Cited by 101 publications

(88 citation statements)

References 43 publications

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“…Many in vitro studies have suggested an important regulatory role for AM in sepsis and other inflammatory diseases [13,18,19,30,33,35]. Moreover, genetic over-expression of AM in the mouse vasculature or therapeutic administration of AM peptide in rats or mice had beneficial effects on reducing the inflammatory and hemodynamic insults elicited by septic shock [28].…”

Section: Discussionmentioning

confidence: 99%

Mice heterozygous for adrenomedullin exhibit a more extreme inflammatory response to endotoxin-induced septic shock

Dackor

Caron

2007

Peptides

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Adrenomedullin (AM) is a highly conserved peptide that can act as a potent vasodilator, antimicrobial factor and anti-inflammatory factor. Several studies have implicated diverse roles for AM in regulating the inflammatory and hemodynamic responses to septic shock. Moreover, during sepsis the receptors that mediate AM signaling [calcitonin receptor-like receptor (calcrl) and receptor activity modifying proteins (RAMP) 2 and 3] undergo dynamic and robust changes in their expression. Although numerous studies have used animal models to study the role of administered or increased AM in septic animals, genetic studies to determine the consequences of reduced AM during septic shock have not yet been performed. Here, we used a murine model of lipopolysaccharide (LPS)-induced septic shock to assess the inflammatory response in mice heterozygous for the AM gene. Following LPS challenge, AM +/− mice had higher expression of TNF-α and IL-1β than LPS-treated wild-type (WT) controls. Consequently, serum TNF-α was also significantly elevated in LPS-treated AM +/− mice compared to WT LPS-treated mice. We also observed higher serum levels of liver enzymes, suggesting more advanced end-organ damage in mice with genetically reduced AM. Finally, we found that RAMP2 and calcrl expression levels were markedly reduced in LPS-treated mice, whereas RAMP3 expression was significantly elevated. Importantly, these changes in receptor gene expression were conserved in AM +/− mice, demonstrating that AM peptide itself does not impact directly on the expression of the genes encoding its receptors. We therefore conclude that during septic shock the dynamic modulation of AM and its receptors primarily functions to dampen the inflammatory response.

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Section: Discussionmentioning

confidence: 99%

Mice heterozygous for adrenomedullin exhibit a more extreme inflammatory response to endotoxin-induced septic shock

Dackor

Caron

2007

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“…Peripheral neuropathy could be due, at least in part, to the induction of proinflammatory cytokines around nerve endings. For example, production by immune cells and/or cancer cells of the proinflammatory cytokines IL-1, IFN-␣, and TNF-␣ can be increased by exposure to paclitaxel, 40,41 cisplatin, 42,43 or irradiation.…”

Section: Preclinical Evidence Consistent With Roles For Cytokines In mentioning

confidence: 99%

“…12 Other preliminary evidence suggested that fatigue is associated with elevations in such proinflammatory cytokines as IL-1, IL-6, TNF-␣, and IFNs. 54 Cell types that are potential sources of cytokines and other immunoregulatory factors in cancer patients include the cancer cells themselves, 41 immune cells (neutrophils, macrophages, lymphocytes), 8,9,40,[42][43][44][45] and nervous system cells (paraganglial cells, glial cells [astrocytes, oligodendrocytes, microglia], and Schwann cells). 6,8,59,60 …”

Section: Clinical Evidence Consistent With Roles For Cytokines In Symmentioning

confidence: 99%

Are the symptoms of cancer and cancer treatment due to a shared biologic mechanism?

Cleeland

Bennett

Dantzer

et al. 2003

Cancer

471

340

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BACKGROUNDCancers and cancer treatments produce multiple symptoms that collectively cause a symptom burden for patients. These symptoms include pain, wasting, fatigue, cognitive impairment, anxiety, and depression, many of which co‐occur. There is growing recognition that at least some of these symptoms may share common biologic mechanisms.METHODSIn November 2001, basic and clinical scientists met to consider evidence for a cytokine‐immunologic model of symptom expression along with directions for future research.RESULTSThe characteristics of cytokine‐induced sickness behavior in animal models have much in common with those of symptomatic cancer patients. Sickness behavior refers to a set of physiologic and behavioral responses observed in animals after the administration of infectious or inflammatory agents or certain proinflammatory cytokines. In some cases, these responses can be prevented by cytokine antagonists. A combination of animal and human research suggests that several cancer‐related symptoms may involve the actions of proinflammatory cytokines.CONCLUSIONSBased on the similarities between cancer symptoms and sickness behavior, the authors discussed approaches to further test the implications of the relationship between inflammatory cytokines and symptoms for both symptom treatment and symptom prevention. Cancer 2003;97:2919–25. © 2003 American Cancer Society.DOI 10.1002/cncr.11382

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“…Several previous studies have suggested that TLR9 is highly expressed in breast cancer cells (9,10). We wondered whether TLR9 has a role in regulating ER·-mediated transactivation of breast cancer directly.…”

Section: Introductionmentioning

confidence: 96%

Toll-like receptor 9 agonist inhibits ERα-mediated transactivation by activating NF-κB in breast cancer cell lines

Qiu

Wang²,

Guo³

et al. 2009

Oncol Rep

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Abstract. Primarily, Toll-like receptor 9 (TLR9) is a specific receptor for microbial DNA in human immune cells. TLR9 has been found to be a promising target in tumor immunotherapy but the direct effect of its activation on tumor cells remains unknown. In this study, we examined the effect of TLR9 ligation on estrogen receptor · (ER·)-mediated transactivation of breast cancer. Luciferase report gene assays, RNA interference of TLR9 and Chromatin immunoprecipitation were performed to measure the effect of TLR9 ligation on ER·-mediated transactivity of T47D and MCF-7 cells. Bromodeoxyuridine incorporation assay was used to examine the effect of TLR9 ligation on estrogen (E2)-induced proliferation of breast cancer cells. We also investigated the mechanism for the effect of TLR9 ligation on ER·-mediated transactivity. We found that ER·-mediated transcription via estrogen response element of human breast cancer cells line T47D was significantly suppressed when treated with 17ß-estradiol in combination with TLR9 agonist CpG oligonucleotides and this effect of CpG was dependent on TLR9. Furthermore, nuclear factor κB (NF-κB) inhibitor BAY 11-7082 could abolish the inhibitory effect of CpG oligonucleotides on ER·-mediated transactivation. We also confirmed the effect of CpG oligonucleotides on ER·-mediated transactivation in the breast cancer cell line MCF-7 forced to stably overexpress TLR9. Finally, we observed that CpG oligonucleotides were also able to inhibit estrogeninduced proliferation of breast cancer cells as a consequence of decreased ER·-mediated transactivation. Taken together, our data suggest that TLR9 signal pathway, by activating NF-κB, negatively regulates ER·-mediated transactivation of breast cancer. Thus, TLR9 agonist inhibits the proliferation of breast cancer cells in response to estrogen.

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INDUCTION OF PROINFLAMMATORY AND CHEMOKINE GENES BY LIPOPOLYSACCHARIDE AND PACLITAXEL (Taxol™) IN MURINE AND HUMAN BREAST CANCER CELL LINES

Cited by 101 publications

References 43 publications

Mice heterozygous for adrenomedullin exhibit a more extreme inflammatory response to endotoxin-induced septic shock

Mice heterozygous for adrenomedullin exhibit a more extreme inflammatory response to endotoxin-induced septic shock

Are the symptoms of cancer and cancer treatment due to a shared biologic mechanism?

Toll-like receptor 9 agonist inhibits ERα-mediated transactivation by activating NF-κB in breast cancer cell lines

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