Fibulins and cancer: friend or foe?

Gallagher, William M.; Currid, Caroline A.; Whelan, Linda C.

doi:10.1016/j.molmed.2005.06.001

Cited by 133 publications

(132 citation statements)

References 36 publications

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“…Others had showed its down-regulation in prostate and gastric cancer [43]. Therefore, speculation still exists regarding FBLN1 as a tumor-suppressor gene or an oncogene or it might even have dual functions [44]. In our study, the over-expression of the FBLN1 protein was observed for good prognosis in EAC.…”

Section: Discussionmentioning

confidence: 46%

Microarray Analysis Reveals Distinct Gene Expression Profiles Among Different Tumor Histology, Stage and Disease Outcomes in Endometrial Adenocarcinoma

et al. 2010

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BackgroundEndometrial cancer is the most common gynecologic malignancy in developed countries and little is known about the underlying mechanism of stage and disease outcomes. The goal of this study was to identify differentially expressed genes (DEG) between late vs. early stage endometrioid adenocarcinoma (EAC) and uterine serous carcinoma (USC), as well as between disease outcomes in each of the two histological subtypes.Methodology/Principal FindingGene expression profiles of 20 cancer samples were analyzed (EAC = 10, USC = 10) using the human genome wide illumina bead microarrays. There was little overlap in the DEG sets between late vs. early stages in EAC and USC, and there was an insignificant overlap in DEG sets between good and poor prognosis in EAC and USC. Remarkably, there was no overlap between the stage-derived DEGs and the prognosis-derived DEGs for each of the two histological subtypes. Further functional annotation of differentially expressed genes showed that the composition of enriched function terms were different among different DEG sets. Gene expression differences for selected genes of various stages and outcomes were confirmed by qRT-PCR with a high validation rate.ConclusionThis data, although preliminary, suggests that there might be involvement of distinct groups of genes in tumor progression (late vs. early stage) in each of the EAC and USC. It also suggests that these genes are different from those involved in tumor outcome (good vs. poor prognosis). These involved genes, once clinically verified, may be important for predicting tumor progression and tumor outcome.

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Section: Discussionmentioning

confidence: 46%

Microarray Analysis Reveals Distinct Gene Expression Profiles Among Different Tumor Histology, Stage and Disease Outcomes in Endometrial Adenocarcinoma

et al. 2010

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“…The value of E relates to the biological function of a macromolecules; the elastic modulus of fibrillar collagen (1,200 MPa), for example, is relatively high reflecting the role of collagen fibrils in resisting tensile forces (Gosline et al 2002), in contrast E for elastin is low (1.1 MPa) (Aaron and Gosline 1981) and a small force will produce a large extension. The elastic modulus of fibrillin microfibrils, however, remains controversial with estimates ranging from 1.0 MPa (Aaron and Gosline 1981) to 96 MPa (Sherratt et al 2003) Gallagher et al 2005;Hubmacher et al 2006;Kielty et al 2002). The MAGPs are small proteins which, in the case of MAGP-1, appear to be essential for the maintenance of microfibril structure (Lemaire et al 2007).…”

Section: Structure and Functionmentioning

confidence: 99%

Tissue elasticity and the ageing elastic fibre

Sherratt

2009

AGE

270

189

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The ability of elastic tissues to deform under physiological forces and to subsequently release stored energy to drive passive recoil is vital to the function of many dynamic tissues. Within vertebrates, elastic fibres allow arteries and lungs to expand and contract, thus controlling variations in blood pressure and returning the pulmonary system to a resting state. Elastic fibres are composite structures composed of a cross-linked elastin core and an outer layer of fibrillin microfibrils. These two components perform distinct roles; elastin stores energy and drives passive recoil, whilst fibrillin microfibrils direct elastogenesis, mediate cell signalling, maintain tissue homeostasis via TGFβ sequestration and potentially act to reinforce the elastic fibre. In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality. This review considers how the unique molecular structure, tissue distribution and longevity of elastic fibres pre-disposes these abundant extracellular matrix structures to the accumulation of damage in ageing dermal, pulmonary and vascular tissues. As compromised elasticity is a common feature of ageing dynamic tissues, the development of strategies to prevent, limit or reverse this loss of function will play a key role in reducing age-related morbidity and mortality.

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“…These interactions may be critical in determining cell movement, proliferation and angiogenesis. Fibulins are believed to have important roles in cancer development because of these diverse interactions (Gallagher et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…FBLN2 is a large 190 kDa protein consisting of four domains, the N-terminal domain, three anaphylatoxin modules, a tandem of epidermal growth factor-like repeats most of which have a calcium-binding domain and the C-terminal fibulin-type module (Gallagher et al, 2005). The third epidermal growth factor-like domain in calcium-binding epidermal growth factor-like repeated modules of FBLN2 is either present or absent as a result of alternative splicing in exon 9; this suggests that both isoforms may be protein coding, as there is only a single deletion of the epidermal growth factor-like domain.…”

Section: Introductionmentioning

confidence: 99%