SOCS-3 antagonises the proliferative and migratory effects of fibroblast growth factor-2 in prostate cancer by inhibition of p44/p42 MAPK signalling

Puhr, Martin; Santer, Frédéric R.; Neuwirt, Hannes; Marcias, Gemma; Hobisch, Alfred; Čulig, Zoran

doi:10.1677/erc-10-0007

Cited by 39 publications

(30 citation statements)

References 51 publications

(65 reference statements)

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“…In addition, the inhibition of MEK1/2 by U0126 suppressed the migration of cholangiocarcinoma cells treated with bFGF. These results are consistent with a recent study that demonstrated the activation of the p44/p42 MAPK pathway, but not the Akt or STAT pathways, following bFGF stimulation (19). To the best of our knowledge, this is the first study to demonstrate the signal transduction pathways of bFGF/FGFR in cholangiocarcinoma cells.…”

Section: Discussionsupporting

confidence: 93%

Basic fibroblast growth factor induces cholangiocarcinoma cell migration via activation of the MEK1/2 pathway

Narong

Leelawat

2011

Oncol Lett

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Abstract. The purpose of this study was to investigate the roles played by basic fibroblast growth factor (bFGF) in the induction of cholangiocarcinoma cell progression and to identify the signal transduction molecules that are activated by bFGF in cholangiocarcinoma cells. FGF receptor-2 (FGFR2) was shown to be expressed in two cholangiocarcinoma cell lines (RMCCA1 and KKU-100). Samples from RMCCA1 and KKU-100 were assayed for the mRNA. Phosphorylation levels were determined by Western blotting. Treatment of the cholangiocarcinoma cells with bFGF enhanced signaling via the phosphorylation of MEK1/2, induced cholangiocarcinoma cell migration and resulted in high levels of actin polymerization. Moreover, treatment with a MEK1/2 inhibitor (U0126) attenuated the effect of bFGF-induced cholangiocarcinoma cell migration. Taken together, these observations indicate that bFGF enhances the migration of cholangiocarcinoma cells and that this enhancement is regulated by the phosphorylation of MEK1/2.

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Section: Discussionsupporting

confidence: 93%

Basic fibroblast growth factor induces cholangiocarcinoma cell migration via activation of the MEK1/2 pathway

Narong

Leelawat

2011

Oncol Lett

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“…The FGF family consists of 23 members (FGF-1-23); FGF-23 was originally identified as a novel member of this FGF family (Puhr et al, 2010) and is generally recognized as a bone-derived protein that is mainly secreted by osteoblasts and osteocytes in adults (Oikonomou et al, 2013). 4015.3 ± 3055.6 3021.0 ± 2388.7* cTnI (ng/mL) 0.3 ± 0.1 0.1 ± 0.1* P 3+ (mM) 2.5 ± 0.8 1.7 ± 0.6* *P < 0.05, compared with PD patients without LVH.…”

Section: Discussionmentioning

confidence: 99%

Role of fibroblast growth factor-23 in the pathogenesis of atherosclerosis in peritoneal dialysis patients

Yin¹,

Feng²,

Han³

et al. 2015

Genet. Mol. Res.

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ABSTRACT.Several previous studies have demonstrated that elevated levels of fibroblast growth factor-23 (FGF-23) may be involved in atherosclerosis and contribute to the high mortality rate of peritoneal dialysis (PD) patients. The aim of this study was to determine the precise role of FGF-23 in the pathogenesis of atherosclerosis in PD patients. Between April 2009 and January 2012, 62 PD patients and 25 control subjects were included in the study. An enzyme-linked immunosorbent assay was conducted to test for plasma FGF-23 levels. Carotid artery intima-media thickness (CIMT), left ventricular mass index (LVMI), and myocardial performance index (MPI) were determined by ultrasonography. Plasma Ca 2+ , P 3+, calcium-phosphorus product, parathyroid hormone, N-terminal pro-brain natriuretic peptide, and cardiac troponin I were also detected. Plasma FGF-23 levels in PD patients were significantly higher than those in control subjects. PD patients with CIMT > 1.0 mm showed the highest levels of FGF-23. Plasma P 3+ , calcium-phosphorous product, plasma parathyroid hormone, CIMT, LVMI, and MPI levels were positively associated with plasma FGF-23 levels. Multiple-stepwise regression analyses revealed that plasma P 3+ , plasma parathyroid hormone, CIMT, LVMI, and MPI levels were strongly associated with plasma FGF-23 levels. However, no correlations were observed in plasma N-terminal probrain natriuretic hormone and cardiac troponin I levels. Plasma FGF-23 levels may play an important role in the initiation and progression of atherosclerosis. Thus, detecting and defining plasma FGF-23 levels may be a promising biomarker for the early detection of atherosclerosis in PD patients.

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“…Down-regulation of SOCS3 causes cell death of prostate cancer through activation of the extrinsic and intrinsic apoptosis pathways [11]. The underlying mechanism is that SOCS3 antagonizes the proliferative and migratory ability in prostate cancer by inhibition of p44/p42 MAPK signaling [12]. In addition, SOCS3 inhibit the signal transducer and activator closely related to Pca cell proliferation and invasiveness, such as transcription 3 (STAT3) [13,14,15], nuclear factor kappa B (NF-κB) [16] and activation protein 1(AP1) [17].…”

Section: Introductionmentioning

confidence: 99%

LXR Agonist Regulates the Carcinogenesis of PCa via the SOCS3 Pathway

Yao

Huang

et al. 2014

Cell Physiol Biochem

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Background: Down-regulation of suppressor of cytokine signaling 3 (SOCS3) inhibits prostate cancer (PCa) cell growth. Liver X receptors (LXRs) agonists have been recently introduced for PCa treatment. We postulated that LXR may inhibit the carcinogenesis of PCa via the SOCS3 pathway. Methods: LNCaP cells were cultured and transfected with SOCS3 small-interfering RNA (SOCS3-siRNA) and control small-interfering RNA (control-siRNA). Then cells were treated with LXR activator (GW3965). The expressions of PCa related transcript factors, e.g. transcription 3 (STAT3), nuclear factor kappa B (NF-κB) and activation protein 1(AP1) were detected by western blot assay. In vitro cell proliferation, cell migration, cell invasion and apoptosis were analysed. Nude mice were used for in vivo tumorgenesis. Results: In cells treated with control-siRNA, GW3965 enhanced SOCS3 expression and significantly inhibited the phosphorylation of STAT3, NF-κB and AP1 expressions, accompanied by dramatically reduced cellular proliferation rate, immigration and invasion of cultured cells. In cells treated with SOCS3-siRNA, the inhibitory effects of LXR activator on the phosphorylation of STAT3 and expressions of NF-κB and AP1 were totally abolished. The cell proliferation rate, immigration and invasion were markedly elevated by SOCS3 gene mutation, even with GW3965 treatment. The in vivo tumorgenesis assay showed that GW3965 significantly reduced the tumor volumes in tumor-bearing nude mice receiving saline injection, but failed to limit the tumor volume in tumor-bearing nude mice receiving SOCS3 antibody injection. Conclusion: Our results provide evidence in support of the notion that LXR agonist may regulate the carcinogenesis of PCa via the SOCS3 pathway.

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SOCS-3 antagonises the proliferative and migratory effects of fibroblast growth factor-2 in prostate cancer by inhibition of p44/p42 MAPK signalling

Cited by 39 publications

References 51 publications

Basic fibroblast growth factor induces cholangiocarcinoma cell migration via activation of the MEK1/2 pathway

Basic fibroblast growth factor induces cholangiocarcinoma cell migration via activation of the MEK1/2 pathway

Role of fibroblast growth factor-23 in the pathogenesis of atherosclerosis in peritoneal dialysis patients

LXR Agonist Regulates the Carcinogenesis of PCa via the SOCS3 Pathway

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