Framing cancer progression: influence of the organ‐ and tumour‐specific matrisome

Rafaeva, Maria; Erler, Janine T.

doi:10.1111/febs.15223

Cited by 29 publications

(25 citation statements)

References 193 publications

(191 reference statements)

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“…All matrix proteins have recently been termed “the matrisome” [ 3 ]. This organ- and context-specific network [ 4 ] is gradually altered throughout tumour initiation [ 5 , 6 , 7 , 8 ], progression and metastasis [ 9 , 10 ] as it provides a niche for tumour cell survival [ 4 , 11 ]. It is considered to be mainly secreted by cancer-associated fibroblasts (CAF) but tumour cells also seem to produce ECM molecules [ 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Expression Profiling of Extracellular Matrix Genes Reveals Global and Entity-Specific Characteristics in Adenoid Cystic, Mucoepidermoid and Salivary Duct Carcinomas

Arolt

Meyer

Hoffmann

et al. 2020

Cancers

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The composition of the extracellular matrix (ECM) plays a pivotal role in tumour initiation, metastasis and therapy resistance. Until now, the ECM composition of salivary gland carcinomas (SGC) has not been studied. We quantitatively analysed the mRNA of 28 ECM-related genes of 34 adenoid cystic (AdCy; n = 11), mucoepidermoid (MuEp; n = 14) and salivary duct carcinomas (SaDu; n = 9). An incremental overexpression of six collagens (including COL11A1) and four glycoproteins from MuEp and SaDu suggested a common ECM alteration. Conversely, AdCy and MuEp displayed a distinct overexpression of COL27A1 and LAMB3, respectively. Nonhierarchical clustering and principal component analysis revealed a more specific pattern for AdCy with low expression of the common gene signature. In situ studies at the RNA and protein level confirmed these results and indicated that, in contrast to MuEp and SaDu, ECM production in AdCy results from tumour cells and not from cancer-associated fibroblasts (CAFs). Our findings reveal different modes of ECM production leading to common and distinct RNA signatures in SGC. Of note, an overexpression of COL27A1, as in AdCy, has not been linked to any other neoplasm so far. Here, we contribute to the dissection of the ECM composition in SGC and identified a panel of deferentially expressed genes, which could be putative targets for SGC therapy and overcoming therapeutic resistance.

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Section: Introductionmentioning

confidence: 99%

Expression Profiling of Extracellular Matrix Genes Reveals Global and Entity-Specific Characteristics in Adenoid Cystic, Mucoepidermoid and Salivary Duct Carcinomas

Arolt

Meyer

Hoffmann

et al. 2020

Cancers

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“…The tight control of cell biochemical and mechanical microenvironment through ECM components like fibronectin, collagen, proteoglycans or laminin is disturbed during the various phases of cancer disease [1]. This leads to ECM remodeling accompanied by increased fiber alignment and matrix stiffening [2]. Adhesion dysregulation is crucial for cancer dissemination and the establishment of metastasis in other tissues with vastly different microenvironments.…”

Section: Introductionmentioning

confidence: 99%

Single-Cell Probe Force Studies to Identify Sox2 Overexpression-Promoted Cell Adhesion in MCF7 Breast Cancer Cells

Iturri

Weber

Vivanco

et al. 2020

Cells

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The replacement of the cantilever tip by a living cell in Atomic Force Microscopy (AFM) experiments permits the direct quantification of cell–substrate and cell–cell adhesion forces. This single-cell probe force measurement technique, when complemented by microscopy, allows controlled manipulation of the cell with defined location at the area of interest. In this work, a setup based on two glass half-slides, a non-fouling one with bacterial S-layer protein SbpA from L. sphaericus CMM 2177 and the second with a fibronectin layer, has been employed to measure the adhesion of MCF7 breast cancer cells to fibronectin films (using SbpA as control) and to other cells (symmetric vs. asymmetric systems). The measurements aimed to characterize and compare the adhesion capacities of parental cells and cells overexpressing the embryonic transcription factor Sox2, which have a higher capacity for invasion and are more resistant to endocrine therapy in vivo. Together with the use of fluorescence techniques (epifluorescence, Total Internal Fluorescence Microscopy (TIRF)), the visualization of vinculin and actin distribution in cells in contact with fibronectin surfaces is enabled, facilitating the monitoring and quantification of the formation of adhesion complexes. These findings demonstrate the strength of this combined approach to assess and compare the adhesion properties of cell lines and to illustrate the heterogeneity of adhesive strength found in breast cancer cells.

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“…54 Detailed review of the role of the ECM in metastasis is beyond the scope of this article and has been reviewed elsewhere. 13 Here, we highlight the role of CAFs and immune cells in regulating ECM remodelling.…”

Section: Key Non-cellular Components In the Tme: The Ecm And Its Remomentioning

confidence: 98%

“…6,10,11 Although the composition of the ECM varies dramatically between cancer types, a common remodelling programme of the ECM and ECM-associated proteins (known as the matrisome) has been suggested to occur during metastasis in multiple solid carcinomas, and the pattern of expression of 22 socalled 'matrisome' genes was shown to be predictive of disease outcome. 12,13 The primary tumour can also direct the formation of a 'pre-metastatic niche' via the systemic release of tumour-derived factors and extracellular vesicles that result in the restructuring and 'priming' of the metastatic site prior to the arrival of tumour cells (reviewed in ref. 14 ).…”

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confidence: 99%

The fibrotic and immune microenvironments as targetable drivers of metastasis

et al. 2020

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Although substantial progress has been made over the past 40 years in treating patients with cancer, effective therapies for those who are diagnosed with advanced metastatic disease are still few and far between. Cancer cells do not exist in isolation: rather, they exist within a complex microenvironment composed of stromal cells and extracellular matrix. Within this tumour microenvironment exists an interplay between the two main stromal cell subtypes, cancer-associated fibroblasts (CAFs) and immune cells, that are important in controlling metastasis. A complex network of paracrine signalling pathways between CAFs, immune cells and tumour cells are involved at multiple stages of the metastatic process, from invasion and intravasation at the primary tumour site to extravasation and colonisation in the metastatic site. Heterogeneity and plasticity within stromal cell populations also contribute to the complexity. Although many of these processes are likely to be common to a number of metastatic sites, we will describe in detail the interplay within the liver, a preferred site of metastasis for many tumours. A greater understanding of these networks provides opportunities for the design of new therapeutic approaches for targeting the metastatic disease.

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Framing cancer progression: influence of the organ‐ and tumour‐specific matrisome

Cited by 29 publications

References 193 publications

Expression Profiling of Extracellular Matrix Genes Reveals Global and Entity-Specific Characteristics in Adenoid Cystic, Mucoepidermoid and Salivary Duct Carcinomas

Expression Profiling of Extracellular Matrix Genes Reveals Global and Entity-Specific Characteristics in Adenoid Cystic, Mucoepidermoid and Salivary Duct Carcinomas

Single-Cell Probe Force Studies to Identify Sox2 Overexpression-Promoted Cell Adhesion in MCF7 Breast Cancer Cells

The fibrotic and immune microenvironments as targetable drivers of metastasis

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