Mitogen-activated protein kinases Erk1/2 and p38 are required for maximal regulation of TIMP-1 by oncostatin M in murine fibroblasts

Li, Tong; Smyth, David; Kerr, Christine; Catterall, J.; Richards, Carl D.

doi:10.1016/j.cellsig.2004.03.003

Cited by 51 publications

(35 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, it is reported that IL-1 induced the activation of ERK-1/2 and p38 MAPK with subsequent increase of the DNA-binding activity of AP-1, but not the activation of JNK and Akt (Hwang et al, 2004). Moreover, IL-1a in the presence of IL-6 inhibited Akt phosphorylation (Tong et al, 2004). Our results in pancreatic cancer cell lines are consistent with these earlier studies, demonstrating that IL-1 had no effect on Akt activation, although the relative contributions of these intracellular signaling pathways appear to vary depending on the cell line and the stimulus used.…”

Section: Discussionmentioning

confidence: 99%

Integrin-linked kinase activity is associated with interleukin-1α-induced progressive behavior of pancreatic cancer and poor patient survival

et al. 2006

View full text Add to dashboard Cite

Cancer cell adhesion and invasion into extracellular matrix are regulated by integrin-linked kinase (ILK) activity in a phosphatidylinositol 3-kinase (PI3-K)-dependent manner.In this study, we demonstrated that ILK and b 1 -integrin play important roles in interleukin (IL)-1a-induced enhancement of adhesion and invasion of pancreatic cancer cells through p38 mitogen-activated protein kinase (MAPK) signaling pathway and activator protein-1 (AP-1) activation. Alteration of ILK kinase activity controlled IL-1a-induced p38 MAPK phosphorylation and its downstream AP-1 activation with subsequent regulation of pancreatic cancer cell adhesion and invasion. Overexpressed ILK enhances the IL-1a-induced p38 MAPK phosphorylation more strongly through glycogen synthase kinase 3 (GSK-3) activation, and subsequently induces AP-1 activation, which promotes aggressive capabilities of pancreatic cancer cells. In contrast, knockdown of ILK kinase activity inhibits the IL-1a-induced activation of MAPK/AP-1 pathway via inhibition of GSK-3 phosphorylation. In immunohistochemical analysis, statistically significant association between strong expression of ILK and poor prognosis of pancreatic cancer patients were observed, and strong expression of ILK in cancerous tissues can be a significant prognostic indicator of pancreatic cancer patients. Our results suggest that ILK is involved with aggressive capability in pancreatic cancer and that these regulations can be helpful to understand biological processes for a better translational treatment for pancreatic cancer patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Integrin-linked kinase activity is associated with interleukin-1α-induced progressive behavior of pancreatic cancer and poor patient survival

et al. 2006

View full text Add to dashboard Cite

show abstract

“…To determine whether anti-OSM treatment was effective, we analyzed BALF levels of IL-6, VEGF, and TIMP-1, three factors known to be induced by OSM stimulation (22). No significant decline in the levels of any of these cytokines was found in the BALF of sensitized and anti-OSM-treated mice, suggesting that OSM neutralization was not effective (Fig.…”

Section: Il-31ra Ko Mice Exhibit Increased Responsiveness To Oncostatmentioning

confidence: 99%

IL-31 Receptor (IL-31RA) Knockout Mice Exhibit Elevated Responsiveness to Oncostatin M

Bilsborough

Mudri²,

Chadwick³

et al. 2010

The Journal of Immunology

View full text Add to dashboard Cite

IL-31 signals through the heterodimeric receptor IL-31RA and oncostatin M receptor (OSMR), and has been linked with the development of atopic dermatitis, a Th2 cytokine-associated disease in humans. However, recent studies of IL-31RA knockout (KO) mice have suggested that IL-31 signaling may be required to negatively regulate Th2 type responses rather than exacerbate them. Because those studies were performed on genetically modified mice, we examined whether neutralizing IL-31 with a specific mAb would give similar results to IL-31RA KO mice in two Th2 cytokine-associated immune models. We report no difference in lymphocyte Th2-type cytokine production after Ag immunization between IL-31RA KO mice, mice treated with the IL-31 mAb, or control animals. Second, we tested whether the absence of the IL-31RA subunit in IL-31RA KO mice may allow for increased pairing of the OSMR subunit with another cytokine receptor, gp130, resulting in overrepresentation of the heterodimeric receptor for OSM and increased responsiveness to OSM protein. We found that intranasal OSM challenge of IL-31RA KO mice resulted in increased IL-6 and vascular endothelial growth factor production in the lung compared with wild-type littermate control animals. Moreover, PBS-challenged IL-31RA KO mice already had increased levels of vascular endothelial growth factor, which were further increased by OSM challenge. These data imply that IL-31RA–deficient mice produce increased levels of OSM-inducible cytokines during airway sensitization and challenge, which may be the driving force behind the apparent exacerbation of Th2-type inflammatory responses previously observed in these mice.

show abstract

“…In view of recent studies demonstrating p38 and p42/44 mitogen-activated protein kinases (MAPK) activation as intracellular signaling pathways leading to induction of TIMP-1 [32,33] as well as findings showing a cannabinoid receptor-dependent activation of MAPKs [3,34,35], our study also assessed a role of both MAPKs in cannabidiol-modulated invasion and TIMP-1 expression. Finally, the impact of cannabidiol on cellular invasion was confirmed by studying metastasis in vivo.…”

Section: Introductionmentioning

confidence: 99%

Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1

Ramer

Merkord

Rohde

et al. 2010

Biochemical Pharmacology

151

149

View full text Add to dashboard Cite

Although cannabinoids exhibit a broad variety of anticarcinogenic effects, their potential use in cancer therapy is limited by their psychoactive effects. Here we evaluated the impact of cannabidiol, a plant-derived non-psychoactive cannabinoid, on cancer cell invasion. Using Matrigel invasion assays we found a cannabidiol-driven impaired invasion of human cervical cancer (HeLa, C33A) and human lung cancer cells (A549) that was reversed by antagonists to both CB 1 and CB 2 receptors as well as to transient receptor potential vanilloid 1 (TRPV1). Additionally, in vivo studies in thymic-aplastic nude mice revealed a significant inhibition of A549 lung metastasis in cannabidiol-treated animals as compared to vehicle-treated controls.Altogether, these findings provide a novel mechanism underlying the anti-invasive action of cannabidiol and imply its use as a therapeutic option for the treatment of highly invasive cancers. Page 3 of 40A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64

show abstract

Mitogen-activated protein kinases Erk1/2 and p38 are required for maximal regulation of TIMP-1 by oncostatin M in murine fibroblasts

Cited by 51 publications

References 50 publications

Integrin-linked kinase activity is associated with interleukin-1α-induced progressive behavior of pancreatic cancer and poor patient survival

Integrin-linked kinase activity is associated with interleukin-1α-induced progressive behavior of pancreatic cancer and poor patient survival

IL-31 Receptor (IL-31RA) Knockout Mice Exhibit Elevated Responsiveness to Oncostatin M

Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1

Contact Info

Product

Resources

About