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Zeng, Y.;  Qiu, Y.;  Jiang, W.;  Fu, B.M. Relationship between Glycocalyx and Tumor Microenvironment. Encyclopedia. Available online: https://encyclopedia.pub/entry/33880 (accessed on 24 April 2024).
Zeng Y,  Qiu Y,  Jiang W,  Fu BM. Relationship between Glycocalyx and Tumor Microenvironment. Encyclopedia. Available at: https://encyclopedia.pub/entry/33880. Accessed April 24, 2024.
Zeng, Ye, Yan Qiu, Wenli Jiang, Bingmei M. Fu. "Relationship between Glycocalyx and Tumor Microenvironment" Encyclopedia, https://encyclopedia.pub/entry/33880 (accessed April 24, 2024).
Zeng, Y.,  Qiu, Y.,  Jiang, W., & Fu, B.M. (2022, November 10). Relationship between Glycocalyx and Tumor Microenvironment. In Encyclopedia. https://encyclopedia.pub/entry/33880
Zeng, Ye, et al. "Relationship between Glycocalyx and Tumor Microenvironment." Encyclopedia. Web. 10 November, 2022.
Relationship between Glycocalyx and Tumor Microenvironment
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The glycocalyx is a fluffy sugar coat covering the surface of all mammalian cells. While glycocalyx at endothelial cells is a barrier to tumor cell adhesion and transmigration, glycocalyx at tumor cells promotes tumor metastasis. Extracellular vesicles (EVs) secreted by the tumor cells and tumor-associated endothelial cells are the components of tumor microenvironment. They can modify glycocalyx of endothelial and tumor cells, as well as tumor vasculature, extracellular matrix (ECM) and fibroblasts. On the other hand, glycocalyx at both cells mediates the secretion and uptake of EVs that affect tumor microenvironment.

extracellular vesicles glycocalyx microenvironment angiogenesis metastasis

1. Introduction

Malignant tumors remain a major threat to human health. Two key challenges facing conventional oncology therapies such as surgery, radiation, and chemotherapy are the local invasion of primary tumors and the metastasis of primary tumors to form secondary tumors, and the development of tumor cell tolerance to therapies [1]. Angiogenesis is a crucial process in tumor growth and progression. In fact, solid tumors do not grow beyond 2–3 mm3 without angiogenesis. Moreover, the vascular system has important functions such as maintaining nutrient and oxygen supply, waste removal, and immune surveillance. Therefore, anti-angiogenic therapies (AATs) that target tumor vasculature to inhibit the growth and metastasis of solid tumors have been widely used in the clinic [2]. However, AATs such as vascular pruning, disruption, and normalization have failed to achieve the desired therapeutic outcomes [1]. After the termination of AATs, the angiogenic process is reactivated and the tumor vascular system is reconstructed, leading to rapid tumor recurrence and metastasis. For example, tumors grow more rapidly in patients with metastatic colorectal cancer after the termination of bevacizumab treatment [3]. Surgical treatments may also increase plasma vascular endothelial growth factor (VEGF) levels and accelerate colorectal cancer growth and metastasis [3]. Discontinuous treatment with bevacizumab promoted tumor growth and revascularization in colorectal cancer xenograft mice [4]. Although sunitinib and bevacizumab reduced microvessel density in the primary tumor tissue of patients with renal cell carcinoma, however, sunitinib promoted endothelial cell (EC) proliferation in tumor tissues [5]. Angiogenesis in tumor growth and tumor progression involves a series of complex changes in the microenvironment. But the mechanism of AAT resistance remains unclear at present. In particular, the mechanisms by which AATs modulate the tumor microenvironment remain unclear.
The tumor microenvironment provides a suitable soil for tumor angiogenesis and growth. Tumor vasculature is disorganized and tortuous, with abnormal vascular ECs and leaky vascular walls. Tumor angiogenesis arises from the stimulation of a complex set of genetic and microenvironmental factors. Interstitial fluid pressure, hypoxia, and acidosis can regulate tumor angiogenesis [6]. EVs are important components of the tumor microenvironment and share many common biological properties, although they can be classified into different types, such as exosomes, apoptotic vesicles, and matrix vesicles, according to their origin and characteristics. EVs perform their biological functions by carrying and transporting ribonucleic acids, proteins, and lipids [7]. EVs are important targets of microenvironmental modification and play an important role in tumor angiogenesis [8]. Compared to normal vascular ECs, tumor ECs are heterogeneous, and AAT can induce tumor ECs to secrete exosomes carrying VEGF, which is defined as VEGF exosomes that could in turn induce angiogenesis and the progression of hepatocellular carcinoma (HCC) [9].
Vascular ECs and their luminal side of the endothelial glycocalyx layer (EGL) are the basic barrier and regulator of material exchange between circulating blood and tissues [10]. Previous studies have shown that the intercellular space between vascular ECs is an important pathway for material exchange in the microcirculation and an important site for tumor cell adhesion and extravasation [11][12][13][14][15]. The EGL also acts as a natural barrier for tumor cells to metastasize across the endothelium [11][12][13][14] and mediates the secretion and uptake of EVs [16][17]. AATs triggered tumor endothelial VEGF exosomes, which are potential modifiers of the tumor stromal microenvironment, are an important linkage between vascular ECs and tumor cells [9]. On the other hand, many components carried by EVs can modify the EGL, which finally facilitates the development of the tumor microenvironment.

2. The Relationship between Glycocalyx and Tumor Microenvironment

The intercellular cleft between vascular ECs is a major pathway for water and hydrophilic molecule exchange in microcirculation and a major site for tumor cell adhesion and transmigration. The endothelial glycocalyx layer is located at the vascular luminal surface, in direct contact with blood, covers the intercellular cleft, and is a natural barrier for tumor cells to metastasize across the vascular wall or endothelium. EGL has a complex structure and is comprised of many components. Heparan sulfate proteoglycan (HSPGs), syndecan-1 (SDC1), syndecan-2 (SDC2), syndecan-4 (SDC4), and glypican-1 (GPC1), and their glycosaminoglycan side chains, including heparan sulfate (HS), hyaluronic acid (HA), and chondroitin sulfate (CS), are important components of EGL [18].
Both vascular endothelial and tumor cells in the tumor microenvironment are involved in tumorigenesis and metastasis. The microenvironmental modification and glycocalyx remodeling of vascular endothelium and tumor cells are prerequisites for tumor angiogenesis, tumor cell invasion, and metastasis. Tumor cell adhesion to and transmigration across the vessel wall are accompanied by the degradation of endothelial glycocalyx and disruption of EC junctions [11][12][13][14]. At the branches and turns of microvessels, the endothelial glycocalyx is more likely to be destroyed by flow-induced factors, which increase vascular permeability and make it easier for tumor cells to adhere to the exposed adhesion molecules either on the ECs or in the ECM [11][12][13][14][15]. In contrast, tumor cell glycocalyx is closely associated with its ability of migration [19]. A most recent study found that a tumor secretion, VEGF, while disrupting the glycocalyx of human cerebral microvascular endothelial cells, significantly enhances heparan sulfate and hyaluronic acid coverage on malignant breast cancer cells MDA-MB-231 [20]. Tumor cell surface glycocalyx promotes the uptake and internalization of EVs [16]. The secretion of syntenin exosomes also requires glycocalyx [21][22]. Disruption of the tumor cell surface glycocalyx reduces the metastatic tumor cells by 95% [19]. These findings suggest that glycocalyx is a potential mediator for vascular endothelium-tumor cell interaction. It is thus important to elucidate the regulatory role of cell surface glycocalyx in tumor microenvironment modulation. Table 1 summarizes the association of glycocalyx components with the tumor microenvironment in various cancers. Before specifying each role of the glycocalyx, the next subsection first reviews the modification of the glycocalyx by the EVs with various cargos.

2.1. Modification of Glycocalyx by EVs

The glycocalyx on different cells may have different changes in response to external stimuli. Vascular ECs co-cultured with tumor cells secrete EVs carrying vascular endothelial cadherin (VE-cadherin), which are reused by tumor cells and promote tumor angiogenesis [8]. VE-cadherin is closely linked to the vascular endothelial glycocalyx. Degradation of the vascular endothelial glycocalyx inhibits circumferential strain-induced VE-cadherin transcription [23], while VE-cadherin knockdown can result in a reduction of the vascular endothelial glycocalyx [24]. Plasma-derived EVs secreted by linoleic acid-induced tumor cells or EVs from the serum of cancer patients promote MMPs secretion and angiogenesis [25]. Previous studies have shown that MMPs can degrade the vascular endothelial glycocalyx [26]. These findings indicate that the glycocalyx can be modified by EVs.
Table 1. Components of glycocalyx and its association with tumor microenvironment.

2.2. Regulation of ECM Remodeling by Glycocalyx

Chemotherapy-driven shedded SDC1 stimulates IL-11 via enhancing HGF/c-met signaling, and it might bind to bone marrow ECM molecules such as collagen and fibronectin, worsening the bone disease in myeloma [27]. SDC1 overexpression in senescent breast stromal fibroblasts induced by ionizing radiation treatment of breast cancer via an autocrine action of TGF-β reduces expression of COL1A1 and increases expression of several MMPs, i.e., MMP-1, -2, -3, and -9 [36]. T47D breast carcinoma cells induce expression of SDC1 in mammary fibroblasts, whereas shedding of SDC1 HS from the fibroblast surface mediates the paracrine growth signal of breast carcinomas [29]. An ECM component, Tenascin-C, which has been reported to compete with the binding sites of fibronectin with SDC4, is recently reported to activate NF-κB signaling by binding with SDC4 to promote tumor progression [37].

2.3. Regulation of Immune Landscape by Glycocalyx

A recent single-cell RNA-seq analysis demonstrated that CCL5-SDC1/4 receptor-ligand interaction mediates the T cells’ crosstalk with tumor cells in pancreatic ductal adenocarcinoma [31]. SDC2 enhances TGF-β signaling in tumor-associated stromal cells and mediates immune evasion in breast cancer [32]. SDC3 expressed on tumor-associated macrophages is promoted by hypoxia inducible factors (HIFs) and might link to a proinflammatory response [33].

2.4. Regulation of Angiogenesis by Glycocalyx

It has been shown that SDC1 promotes the transformation of tumor ECs into an angiogenic phenotype [34]. SDC1 silencing inhibits the organization of tumor ECs into patent vessels in severe combined immunodeficient (SCID) mice, reduces membrane expression of VEGFR2, and thus weakens the colocalization of VEGFR2 with SDC1 [34]. SDC2 is closely associated with cytoskeleton organization, integrin signaling, and developmental angiogenesis, and is required for the development of the vascular system. SDC2 promotes VEGF/VFGFR2 complex formation and VEGF-dependent neovascularization [38]. Global and inducible endothelial-specific deletion of SDC2 in mice markedly impairs VEGF signaling and leads to angiogenic defects [38]. The shed SDC2 enhances tumorigenic activity by increasing the crosstalk of cancer cells with tumor-associated macrophages and endothelial cells to enhance angiogenesis for colon cancer progression via producing VEGF [35]. VEGF is a central effector of angiogenesis and vascular permeability regulated by EVs. VEGF also activates MMPs [39], which can degrade the vascular endothelial glycocalyx [26]. The interplay among VEGF, MMPs, and endothelial glycocalyx is still unclear.
Moreover, whether vascular endothelial glycocalyx participates in the tumor angiogenesis and tumor metastasis remains unclear. Further investigation is required. VEGF not only selectively regulates the proliferation and motility of vascular ECs but also enhances vascular permeability, leading to fibrin gel deposition and providing a suitable microenvironment for tumor metastasis [40]. VEGF can disrupt EC junctions, promote the adhesion of tumor cells to microvessels, and enhance microvascular permeability through the VEGF receptor 2 (VEGFR2/FDR/Flk-1) pathway [14][41]. The role of the VEGFR2 pathway in mediating the disruption of vascular endothelial glycocalyx and cell junctions has attracted much attention recently.

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