The role of putative intragenic control elements in c-fos regulation by calcium and growth factor signalling pathways

2001 ◽  
Vol 77 (5) ◽  
pp. 1293-1300 ◽  
Author(s):  
Claudia M. Lange ◽  
Hilmar Bading
Keyword(s):  
Growth Factor ◽  
Signalling Pathways ◽  
Growth Factor Signalling

scholarly journals The Role of Suppressors of Cytokine Signalling in Human Neoplasms

2014 ◽  
Vol 2014 ◽  
pp. 1-24 ◽  
Author(s):  
Walid Sasi ◽  
Anup K. Sharma ◽  
Kefah Mokbel
Keyword(s):  
Growth Factor ◽  
Negative Feedback ◽  
Signalling Pathways ◽  
Solid Organ ◽  
Haematological Malignancies ◽  
Biological Functions ◽  
Tumour Suppressors ◽  
Intracellular Proteins ◽  
Growth Factor Signalling

Suppressors of cytokine signalling 1–7 (SOCS1–7) and cytokine-inducible SH2-containing protein (CIS) are a group of intracellular proteins that are well known as JAK-STAT and several other signalling pathways negative feedback regulators. More recently several members have been identified as tumour suppressors and dysregulation of their biological roles in controlling cytokine and growth factor signalling may contribute to the development of many solid organ and haematological malignancies. This review explores their biological functions and their possible tumour suppressing role in human neoplasms.

scholarly journals Activation of multiple growth factor signalling pathways is frequent in meningiomas

2015 ◽  
Vol 36 (3) ◽  
pp. 250-261 ◽  
Author(s):  
David A Hilton ◽  
Aditya Shivane ◽  
Leanne Kirk ◽  
Kayleigh Bassiri ◽  
Doyo G Enki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Signalling Pathways ◽  
Growth Factor Signalling

Control of growth factor signalling by MACPF proteins

2019 ◽  
Vol 47 (3) ◽  
pp. 801-810
Author(s):  
Daniel Bakopoulos ◽  
James C. Whisstock ◽  
Travis K. Johnson
Keyword(s):  
Cell Death ◽  
Growth Factor ◽  
Membrane Attack Complex ◽  
Fruit Fly ◽  
Mechanisms Of Action ◽  
Signalling Pathways ◽  
Growth Factor Signalling ◽  
Macpf Domain ◽  
Apoptotic Factors ◽  
Unique Ability

AbstractMembers of the membrane attack complex/perforin-like (MACPF) protein superfamily have long captured interest because of their unique ability to assemble into large oligomeric pores on the surfaces of cells. The best characterised of these act in vertebrate immunity where they function to deliver pro-apoptotic factors or induce the cytolysis and death of targeted cells. Less appreciated, however, is that rather than causing cell death, MACPF proteins have also evolved to control cellular signalling pathways and influence developmental programmes such as pattern formation and neurogenesis. Torso-like (Tsl) from the fruit fly Drosophila, for example, functions to localise the activity of a growth factor for patterning its embryonic termini. It remains unclear whether these developmental proteins employ an attenuated form of the classical MACPF lytic pore, or if they have evolved to function via alternative mechanisms of action. In this minireview, we examine the evidence that links pore-forming MACPF proteins to the control of growth factor and cytokine signalling. We will then attempt to reconcile how the MACPF domain may have been repurposed during evolution for developmental events rather than cell killing.

Cracking the mild, difficult and fiendish codes within and downstream of the EGFR to link diagnostics and therapeutics

2007 ◽  
Vol 35 (1) ◽  
pp. 1-6 ◽  
Author(s):  
M. Waterfield
Keyword(s):  
Signal Transduction ◽  
Growth Factors ◽  
Growth Factor ◽  
Signalling Pathways ◽  
Growth Factor Signalling ◽  
Transduction Mechanisms

Over the last 45 years, I have been working on growth factors, their receptors and signal transduction mechanisms. This period has seen a tremendous growth in knowledge and technology, and all of this, together with a focus interest in oncology, has steered me along a path designed to understand growth factor signalling so that we can see how drugs that target signalling pathways might be able to control cancer. The knowledge that we already have is likely to lead to cures for many common cancers within the next 25 years.

scholarly journals Tumour initiating cells and IGF/FGF signalling contribute to sorafenib resistance in hepatocellular carcinoma

Gut ◽  
2015 ◽  
Vol 66 (3) ◽  
pp. 530-540 ◽  
Author(s):  
Victoria Tovar ◽  
Helena Cornella ◽  
Agrin Moeini ◽  
Samuel Vidal ◽  
Yujin Hoshida ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Growth Factor ◽  
Molecular Mechanisms ◽  
Acquired Resistance ◽  
Gene Signature ◽  
Signalling Pathways ◽  
Fgf Signalling

ObjectiveSorafenib is effective in hepatocellular carcinoma (HCC), but patients ultimately present disease progression. Molecular mechanisms underlying acquired resistance are still unknown. Herein, we characterise the role of tumour-initiating cells (T-ICs) and signalling pathways involved in sorafenib resistance.DesignHCC xenograft mice treated with sorafenib (n=22) were explored for responsiveness (n=5) and acquired resistance (n=17). Mechanism of acquired resistance were assessed by: (1) role of T-ICs by in vitro sphere formation and in vivo tumourigenesis assays using NOD/SCID mice, (2) activation of alternative signalling pathways and (3) efficacy of anti-FGF and anti-IGF drugs in experimental models. Gene expression (microarray, quantitative real-time PCR (qRT-PCR)) and protein analyses (immunohistochemistry, western blot) were conducted. A novel gene signature of sorafenib resistance was generated and tested in two independent cohorts.ResultsSorafenib-acquired resistant tumours showed significant enrichment of T-ICs (164 cells needed to create a tumour) versus sorafenib-sensitive tumours (13 400 cells) and non-treated tumours (1292 cells), p<0.001. Tumours with sorafenib-acquired resistance were enriched with insulin-like growth factor (IGF) and fibroblast growth factor (FGF) signalling cascades (false discovery rate (FDR)<0.05). In vitro, cells derived from sorafenib-acquired resistant tumours and two sorafenib-resistant HCC cell lines were responsive to IGF or FGF inhibition. In vivo, FGF blockade delayed tumour growth and improved survival in sorafenib-resistant tumours. A sorafenib-resistance 175 gene signature was characterised by enrichment of progenitor cell features, aggressive tumorous traits and predicted poor survival in two cohorts (n=442 patients with HCC).ConclusionsAcquired resistance to sorafenib is driven by T-ICs with enrichment of progenitor markers and activation of IGF and FGF signalling. Inhibition of these pathways would benefit a subset of patients after sorafenib progression.

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