Matrix, Extracellular and Interstitial

Akalu, Abebe; Brooks, Peter C.

doi:10.1002/3527600906.mcb.200400091

Cited by 7 publications

(20 citation statements)

References 179 publications

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“…The non‐cellular solid‐state structural compartment of the tumor microenvironment or ECM plays a critical role in controlling tumor metastasis. In general, the ECM can be organized into two major subdivisions including the loosely arranged interstitial matrix and the basement membrane or basal lamina (Akalu and Brooks, 2005). The acellular ECM is composed of a wide array of structural and regulatory molecules including a number of proteogylcan and large multi‐domain glycoproteins.…”

Section: The Non‐cellular Solid‐state Structural Compartment In the Tmentioning

confidence: 99%

“…The acellular ECM is composed of a wide array of structural and regulatory molecules including a number of proteogylcan and large multi‐domain glycoproteins. In addition to the major glycoproteins of collagen, laminin, and fibronectin, a number of secreted soluble factors such as protease inhibitors, growth factors, cytokines, chemokines, and matricellular proteins are imbedded within the mesh like network of the ECM (Akalu and Brooks, 2005). Given the complexity of the interconnected ECM, it would be well beyond the scope of the current review to discus in detail all the components that comprise the ECM and how each impacts the metastastic cascade.…”

Section: The Non‐cellular Solid‐state Structural Compartment In the Tmentioning

confidence: 99%

“…In this regard, a hallmark of malignant tumor progression involves proteolytic remodeling of the ECM. In addition, altered patterns of glycoslyation, and differential gene splicing contribute to the expression of molecules with distinct conformations that may be unique to the tumor microenvironment (Brooks, 2002; Akalu and Brooks, 2005, 2007; Akalu et al, 2005). Given this possibility, cellular response to this altered tumor microenvironment likely initiates unique sets of signaling cascades as compared to cellular communication with the intact ECM molecules in normal tissue microenvironments.…”

Section: Bi‐directional Cellular Communication With Solid‐state Ecm Cmentioning

confidence: 99%

“…While some have argued that vitronectin is not a major structural ECM protein, it has been found within a number of tissues and within the ECM of many malignant tumors (Tomasini and Mosher, 1988; Akalu and Brooks, 2005). This multifunctional glycoprotein plays important roles in the coagulation cascade, binds and regulates bioavailability of certain growth factors and modulates cell adhesion, migration, proliferation, and survival (Tomasini and Mosher, 1988; Akalu and Brooks, 2005). Elevated levels of vitronectin may help facilitate brain tumor invasion and blocking integrin‐mediated interactions with vitronectin can inhibit tumor cell adhesion and invasion (Uhm et al, 1999).…”

Section: Cryptic Vitronectin Elements Within the Non‐cellular Tumor Mmentioning

confidence: 99%

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Impact of the non‐cellular tumor microenvironment on metastasis: Potential therapeutic and imaging opportunities

Cretu

Brooks

2007

Journal Cellular Physiology

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Evidence is accumulating that the malignant phenotype of a given tumor is dependent not only on the intrinsic characteristics of tumor cells, but also on the cooperative interactions of non-neoplastic cells, soluble secreted factors and the non-cellular solid-state ECM network that comprise the tumor microenvironment. Given the ability of the tumor microenvironment to regulate the cellular phenotype, recent efforts have focused on understanding the molecular mechanisms by which cells sense, assimilate, interpret, and ultimately respond to their immediate surroundings. Exciting new studies are beginning to unravel the complex interactions between the numerous cell types and regulatory factors within the tumor microenvironment that function cooperatively to control tumor cell invasion and metastasis. Here, we will focus on studies concerning a common theme, which is the central importance of the non-cellular solid-state compartment as a master regulator of the malignant phenotype. We will highlight the non-cellular solid-state compartment as a relatively untapped source of therapeutic and imaging targets and how cellular interactions with these targets may regulate tumor metastasis.

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Section: The Non‐cellular Solid‐state Structural Compartment In the Tmentioning

confidence: 99%

Section: The Non‐cellular Solid‐state Structural Compartment In the Tmentioning

confidence: 99%

Section: Bi‐directional Cellular Communication With Solid‐state Ecm Cmentioning

confidence: 99%

Section: Cryptic Vitronectin Elements Within the Non‐cellular Tumor Mmentioning

confidence: 99%

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Impact of the non‐cellular tumor microenvironment on metastasis: Potential therapeutic and imaging opportunities

Cretu

Brooks

2007

Journal Cellular Physiology

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“…The ECM was originally thought to function only as a mechanical support to cells and tissues but this concept has changed in the past years with findings that the ECM contains a wealth of biochemical information with importance for cellular processes including adhesion, migration, and proliferation (1). The perivascular ECM is particularly involved in angiogenesis, a process involving the formation of new blood vessels from preexisting vasculature occurring during physiologic and pathologic conditions, including tumor growth and metastasis (2)(3)(4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Novel anti-denatured collagen humanized antibody D93 inhibits angiogenesis and tumor growth: An extracellular matrix-based therapeutic approach

Pernasetti¹,

Nickel²,

Clark³

et al. 2006

Int J Oncol

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Abstract. Matrix metalloproteases (MMPs) secreted by both tumor and endothelial cells proteolytically degrade collagen during tumor growth and neo-vascularization. This exposes cryptic binding sites on collagen with functional relevance for angiogenesis. In this report, we characterized a novel humanized monoclonal IgG1 antibody, D93. After humanization, the antibody retained the binding specificity of the parental murine IgM antibody for denatured (dn) collagen. D93 recognized dn-collagen but not native (nat) collagen of different species, including mouse, chicken, and human, indicating that its cryptic binding site(s) is conserved across species. In immunohistochemistry (IHC) studies, D93 stained the basement membrane of blood vessels in several xenograft human tumors or in surgically removed tumor tissues from patients with different types of malignancies. D93 staining was rarely or not present in normal blood vessels of healthy tissues. In in vivo experiments, D93 significantly inhibited basic fibroblast growth factor (bFGF)-induced angiogenesis in chick embryo chorioallantoic membrane (CAM) and the tumor growth of pre-established orthotopic human breast (MDA-MB-435) tumors in mice. D93 i.v. administered in mice was subsequently detected in the subendothelial basement membrane of tumor blood vessels but not blood vessels of normal tissues. Inhibition of growth of pre-established orthotopic human breast MDA-MB-435 tumors was more effective when D93 was combined with Taxol, than either treatment alone. In addition, tumors from animals treated with D93 and/or Taxol showed significantly reduced levels of the endothelial cell-marker CD31. Our data suggest that blockade of cryptic epitopes exposed on collagen IV during angiogenesis and tumor growth by a monoclonal antibody may provide a novel therapeutic modality for treatment of cancer and pathogenic neo-vascularization.

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Polymer Hydrogels to Guide Organotypic and Organoid Cultures

Magno

Meinhardt

Werner

2020

Adv Funct Materials

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Human organotypic and organoid cultures provide increasingly lifelike models of tissue/organ development and disease, enable more realistic drug screening, and may ultimately pave the way for new therapies. A broad variety of extracellular matrix-based or inspired materials is instrumental in these approaches. In this review article, the foundations of the related materials design are summarized with an emphasis on the advantages and limitations of decellularized and reconstituted biopolymeric matrices as well as biohybrid and fully synthetic polymer hydrogel systems applied to enable specific organotypic and organoid cultures. Recent progress in the fabrication of defined hydrogel systems offering thoroughly tunable biochemical and biophysical properties is highlighted. Potentialities of hydrogel-based approaches to address the persisting challenges of organoid technologies, namely scalability, connectivity/integration, reproducibility, parallelization, and in situ monitoring are discussed.

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Matrix, Extracellular and Interstitial

Cited by 7 publications

References 179 publications

Impact of the non‐cellular tumor microenvironment on metastasis: Potential therapeutic and imaging opportunities

Impact of the non‐cellular tumor microenvironment on metastasis: Potential therapeutic and imaging opportunities

Novel anti-denatured collagen humanized antibody D93 inhibits angiogenesis and tumor growth: An extracellular matrix-based therapeutic approach

Polymer Hydrogels to Guide Organotypic and Organoid Cultures

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