Level of plasma fibronectin in patients with breast cancer

Ruelland, A.; Kerbrat, Pierre; Clerc, Christian; Legras, B; Cloarec, L

doi:10.1016/0009-8981(88)90236-7

Cited by 14 publications

(10 citation statements)

References 8 publications

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“…Basement membrane breach exposes epithelial cells to the stromal ECM, and our results support the idea that cell-stromal interactions have a synergistic role in promoting a change in cell phenotype such as EMT. Up-regulation of FN expression by cancer-associated fibroblasts (36) or transport into the tissue of FN, which can be increased in the plasma in breast cancer (37) are two ways in which stromal FN levels could be elevated. Our results showing cell stimulation by FN when levels of TGFβ are sub-threshold indicate that an up-regulation of FN in tissue could impact the rate of tumor formation.…”

Section: Discussionmentioning

confidence: 99%

Mammary epithelial cell interactions with fibronectin stimulate epithelial-mesenchymal transition

2013

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In the mammary gland, the stromal extracellular matrix (ECM) undergoes dramatic changes during development and in tumorigenesis. For example, normal adult breast tissue is largely devoid of the ECM protein fibronectin (FN) whereas high FN levels have been detected in the stroma of breast tumors. FN is an established marker for epithelial-mesenchymal transition (EMT), which occurs during development and has been linked to cancer. During EMT, epithelial cell adhesion switches from cell-cell contacts to mainly cell-ECM interactions raising the possibility that FN may have a role in promoting this transition. Using MCF-10A mammary epithelial cells, we show that exposure to exogenous FN induces an EMT response including up-regulation of the EMT markers FN, Snail, N-cadherin, vimentin, the matrix metalloprotease MMP2, α-smooth muscle actin, and phospho-Smad2 as well as acquisition of cell migratory behavior. FN-induced EMT depends on Src kinase and ERK/MAP kinase signaling but not on the immediate early gene EGR-1. FN initiates EMT under serum-free conditions; this response is partially reversed by a TGFβ neutralizing antibody suggesting that FN enhances the effect of endogenous TGFβ. EMT marker expression is up-regulated in cells on a fragment of FN containing the integrin-binding domain but not other domains. Differences in gene expression between FN and MG are maintained with addition of a sub-threshold level of TGFβ1. Together, these results show that cells interacting with FN are primed to respond to TGFβ. The ability of FN to induce EMT shows an active role for the stromal ECM in this process and supports the notion that the increased levels of FN observed in breast tumors facilitate tumorigenesis.

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Section: Discussionmentioning

confidence: 99%

Mammary epithelial cell interactions with fibronectin stimulate epithelial-mesenchymal transition

2013

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“…The level of plasma FN1 varied in different cancers. Depleted plasma FN1 levels were observed in chronic lymphocytic leukemia and osteomyelosclerosis [23], whereas elevated plasma FN1 levels were found in breast cancer [24] and gastric cancer [25]. The role of FN1 in tumorigenesis and malignant progression has been highly controversial [26].…”

Section: Discussionmentioning

confidence: 99%

Glycoproteomic Analysis Reveals Aberrant Expression of Complement C9 and Fibronectin in the Plasma of Patients with Colorectal Cancer

et al. 2020

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Colorectal cancer (CRC) is a major cause of cancer mortality. Currently used CRC biomarkers provide insufficient sensitivity and specificity; therefore, novel biomarkers are needed to improve the CRC detection. Label-free quantitative proteomics were used to identify and compare glycoproteins, enriched by wheat germ agglutinin, from plasma of CRC patients and age-matched healthy controls. Among 189 identified glycoproteins, the levels of 7 and 15 glycoproteins were significantly altered in the non-metastatic and metastatic CRC groups, respectively. Protein-protein interaction analysis revealed that they were predominantly involved in immune responses, complement pathways, wound healing and coagulation. Of these, the levels of complement C9 (C9) was increased and fibronectin (FN1) was decreased in both CRC states in comparison to those of the healthy controls. Moreover, their levels detected by immunoblotting were validated in another independent cohort and the results were consistent with in the study cohort. Combination of CEA, a commercial CRC biomarker, with C9 and FN1 showed better diagnostic performance. Interestingly, predominant glycoforms associated with acetylneuraminic acid were obviously detected in alpha-2 macroglobulin, haptoglobin, alpha-1-acid glycoprotein 1, and complement C4-A of CRC patient groups. This glycoproteomic approach provides invaluable information of plasma proteome profiles of CRC patients and identification of CRC biomarker candidates.

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“…It is additionally interesting to note that 14/18 of the upregulated protein-validated factors are associated with poor prognosis or invasion in breast cancers, when measured in serum or tissue; this suggests that cells which secrete these factors would have a negative impact on prognosis 39,41,47,49,54,[56][57][58][59][60][61][62][63][64][65][66][67][68][69][70][71][72] . It is also of interest to note that in these studies 8/14 of these poorly prognostic factors have been seen to derive predominantly from stromal cells.…”

Section: Discussionmentioning

confidence: 99%

Cancer-associated hypersialylated MUC1 drives the differentiation of monocytes into macrophages with a pathogenic phenotype

Beatson

Graham

Grundland-Freile

et al. 2020

Preprint

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The tumour microenvironment plays a crucial role in the growth and progression of cancer and the presence of tumour-associated macrophages (TAMs) is associated with poor prognosis. Recent studies show that TAMs show transcriptomic, phenotypic, functional and geographical diversity. Here we show that a sialylated tumour-associated glycoform of the mucin MUC1, MUC1-ST, through the engagement of Siglec-9 can specifically and independently induce the differentiation of monocytes into TAMs with a unique phenotype.These TAMs can recruit and maintain neutrophils, inhibit the function of T cells, degrade

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Level of plasma fibronectin in patients with breast cancer

Cited by 14 publications

References 8 publications

Mammary epithelial cell interactions with fibronectin stimulate epithelial-mesenchymal transition

Mammary epithelial cell interactions with fibronectin stimulate epithelial-mesenchymal transition

Glycoproteomic Analysis Reveals Aberrant Expression of Complement C9 and Fibronectin in the Plasma of Patients with Colorectal Cancer

Cancer-associated hypersialylated MUC1 drives the differentiation of monocytes into macrophages with a pathogenic phenotype

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