Prominent collagen type VI expression in juvenile angiofibromas

Gramann, Monika; Wendler, Olaf; Haeberle, Lothar; Schick, Bernhard

doi:10.1007/s00418-008-0501-0

Cited by 17 publications

(22 citation statements)

References 33 publications

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“…RNA extraction and quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) were performed as described previously [14,15]. Illustra™ Mini RNA Isolation Kit (GE Healthcare, Buckinghamshire, UK) was used according to the manufacturer's instructions for isolation.…”

Section: Methodsmentioning

confidence: 99%

Nicotinic Acetylcholine Receptors in Head and Neck Cancer and Their Correlation to Tumor Site and Progression

Scherl

Schäfer²,

Schlabrakowski³

et al. 2016

ORL

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Background: Nicotine contributes to tumorigenesis through stimulation of nicotinic acetylcholine receptors (nAChRs) in head and neck squamous cell carcinoma (SCC). Although many factors have been found to be involved in the pathogenesis of head and neck cancer, the effect of nAChRs is still unclear. The study provides information on different subtypes in SCC and normal mucosa (NM) and their clinicopathological correlation to tumor progression. Methods: SCC (n = 34) of oropharynx, hypopharynx, larynx and corresponding NM (n = 38) were analyzed by quantitative real-time polymerase chain reaction, immunoblotting and immunohistochemistry and correlated to tumor grading and Union for International Cancer Control (UICC) stage. Results: nAChR subtypes α1, α3, α5 and α7 were found in NM and SCC of the upper aerodigestive tract with high rates of α1 and α5 in SCC. An overexpression of α1 was found in laryngeal and hypopharyngeal SCC, while α3 and α7 subunits were downregulated. The expression of α1 and α5 subunits increased with tumor progression. Conclusion: The nAChR subunit pattern shows a difference between NM and SCC and changes in the process of tumor progression. Therefore, it is conceivable that it contributes to tumorigenesis. The findings provide a basis for further studies in prognostic assessment and identifying carcinogenic changes from NM to SCC.

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Section: Methodsmentioning

confidence: 99%

Nicotinic Acetylcholine Receptors in Head and Neck Cancer and Their Correlation to Tumor Site and Progression

Scherl

Schäfer²,

Schlabrakowski³

et al. 2016

ORL

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“…On the contrary, ST3 exhibits a collagenolytic function against the native α3 chain of collagen VI (38). Prominent collagen-type VI expression has been previously described in JNA vessels, possibly exerting growth stimulatory effects on endothelial cells (6,7).…”

Section: Discussionmentioning

confidence: 91%

“…The presence of proteins such as merosin (laminin α2) and collagens type VI and 1A2, which were recently described as being highly expressed in JNA vessels, is suggestive of vessels in an early developmental vascular differentiation state (5)(6)(7). Notably, merosin and type VI collagen were also elevated in several types of cancer and in proliferative hemangiomas.…”

Section: Introductionmentioning

confidence: 93%

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Markers of vascular differentiation, proliferation and tissue remodeling in juvenile nasopharyngeal angiofibromas

Nonogaki

Campos

Butugan

et al. 2010

Experimental and Therapeutic Medicine

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Abstract. Juvenile nasopharingeal angiofibroma (JNA) is a histologically benign locally aggressive tumor characterized by irregular vessels embedded in a fibrous stroma. Excessive vascularity results in bleeding complications, and the inhibition of angiogenesis is a promising strategy for managing extensive JNA tumors. To better characterize the endothelial components of JNA, we aimed to evaluate markers of vascular differentiation and proliferation, such as friend leukemia integration-1 (FLI-1) and endoglin, lymphatic markers, including podoplanin and vascular endothelial growth factor receptor 3 (VEGFR3) and its cognate ligand VEGFC, GLUT-1, a diagnostic marker that discriminates between hemangiomas and vascular malformations, and two markers of tissue remodeling, stromelysin 3 (ST3) and secreted acid protein rich in cysteine (SPARC). Antigens were assessed immunohistochemically in vessels and stromal cells of JNA archival cases (n=22). JNA endothelial cells were positive for endoglin, VEGFC and FLI-1, whereas podoplanin and VEGFR3 were negative in all cases. Both endothelial cells and fibroblasts stained for ST3 and SPARC. GLUT-1 was investigated in JNA cases, in infantile hemangiomas (n=123) and in vascular malformations (n=135) as controls. JNAs and vascular malformations were GLUT-1-negative, while hemangiomas showed positive staining. The presence of markers of endothelial differentiation and proliferation highlighted the hyper-proliferative state of JNA vessels. The absence of podoplanin and VEGFR3 underscores their blood endothelial cell characteristic. The absence of GLUT-1 discriminates JNAs from hemangiomas. ST3 and SPARC up-regulation in endothelial cells and fibroblasts may contribute to a compensatory signaling for controlling angiogenesis. Some of these markers may eventually serve as therapeutic targets. Our results may aid in the understanding of JNA pathophysiology.

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“…A set of refined experiments by using α4β1integrin-subunit have demonstrated that NG2/CSPG4 interacts with the α4β1integrin-subunit modulated-cell adhesion to type VI collagens [52]. Adhesion to the collagens of the cancer cell matrix "wakes up" cancer cells, which allows integrins to form associations with various signal transduction molecules such as Focal Adhesion Kinase (FAK).…”

Section: Activated Ng2/cspg4 Proteoglycan In Cancer Cell Adhesion (Camentioning

confidence: 99%

NG2/CSPG4 Proteoglycan as a Novel Prognostic Indicator and Therapeutic Target in Malignant Cancer

Bie¹

2014

J Stem Cell Res Ther

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This review article describes the interaction of Neuron-glia 2 Chondroitin Sulfate Proteoglycan 4 (NG2/CSPG4) in cancer cell matrix, and its role within the cancer cell matrix in promoting angiogenesis and its potential clinical use as a novel immune drug target. Malignant cancer is maintained by a cross-talk between the cancer cells and cancer cell matrix where the activated cancer cell matrix nurtures the advancing cancer cells by providing Extracellular Matrix (ECM), neovasculature and stimulatory growth factors. Researches in recent years have accumulated a wealth of novel insight into mechanisms by which how cancer cells are co-evolved with activated cancer cell matrix throughout cancer settings. Currently, the cancer cell matrix is considered as an important "effector" in carcinogenesis. Once tightly defined cell matrix in normal tissue occasionally becomes sabotaged, the inevitable malignant progression will flip on. NG2/CSPG4 is a big multifunctional transmembrane proteoglycan with limited expression in normal tissues and its unparalleled structural-functional diversity endows it with the ability to serve as critical mediator. We describe here how the manipulation of NG2/CSPG4 on the processes driving malignant cancer cell matrix activation promotes carcinogenesis through the alteration of cancer cell adhesion, infiltration, migration, proliferation and angiogenesis, and how it will be possibile to design a decisive strategy for the development of a novel therapy specifically targeting this macromolecule for malignant cancer treatment.

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Prominent collagen type VI expression in juvenile angiofibromas

Cited by 17 publications

References 33 publications

Nicotinic Acetylcholine Receptors in Head and Neck Cancer and Their Correlation to Tumor Site and Progression

Nicotinic Acetylcholine Receptors in Head and Neck Cancer and Their Correlation to Tumor Site and Progression

Markers of vascular differentiation, proliferation and tissue remodeling in juvenile nasopharyngeal angiofibromas

NG2/CSPG4 Proteoglycan as a Novel Prognostic Indicator and Therapeutic Target in Malignant Cancer

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