Collagen XVI expression is upregulated in glioblastomas and promotes tumor cell adhesion

Senner, Volker; Ratzinger, Sabine; Mertsch, Sonja; Grässel, Susanne; Paulus, Werner

doi:10.1016/j.febslet.2008.09.017

Cited by 51 publications

(47 citation statements)

References 19 publications

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“…We demonstrated a strong upregulation of collagen XVI in glioblastoma tissue, which is characterized by aggressive tumour cell invasion into its surrounding tissue. Using glioma cell lines as model system we observed that collagen XVI ameliorates adhesion of these cells to matrix with the glioma cell line U87MG showing strongest adhesion on collagen XVI among all tested glioma cell lines [11].…”

Section: Introductionmentioning

confidence: 91%

“…5x10 5 cells per reaction were incubated with 80 pmol of siRNA (8pmol / μl) and 100 μl Nucleofector solution and run on program X-01. The cells were transfected with two collagen XVI-specific siRNAs: siRNA1 (5'-uga gcu cau uga gau caa u dTdT-3') and siRNA2 (5'-gga cuc aaa uug gaa cac a dTdT-3') and the corresponding sequences as double strand; as well as scrambled siRNA (control) as described elsewhere [11]. All siRNAs were purchased from Qiagen, Hilden, Germany.…”

Section: Transfectionmentioning

confidence: 99%

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Inhibition of Collagen XVI Expression Reduces Glioma Cell Invasiveness

Bauer¹,

Ratzinger²,

Wales³

et al. 2011

Cell Physiol Biochem

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Glioblastomas are characterized by an intense local invasiveness that limits surgical resection. One mechanism by which glioma cells enforce their migration into brain tissue is reorganization of tumour associated extracellular matrix (ECM). Collagen XVI is a minor component of connective tissues. However, in glioblastoma tissue it is dramatically upregulated compared to the ECM of normal cortex. The aim of this study is to delineate tumour cell invasion and underlying mechanisms involving collagen XVI by using a siRNA mediated collagen XVI knockdown model in U87MG human glioblastoma cells. Knockdown of collagen XVI resulted in decreased invasiveness in Boyden chamber assays, and in a reduction of focal adhesion contact numbers per cell. Gene expression was upregulated for protocadherin 18 and downregulated for kindlin-1 and -2. Proliferation was not affected while flow cytometric analysis demonstrated reduced β1-integrin activation in collagen XVI knockdown cells. We suggest that in glioblastoma tissue collagen XVI may impair the cell-cell interaction in favour of enhancement of invasion. The modification of the β1-integrin activation pattern through collagen XVI might be a molecular mechanism to further augment the invasive phenotype of glioma cells. Elucidating the underlying mechanisms of glioma cell invasion promoted by collagen XVI may provide novel cancer therapeutic approaches in neurooncology.

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Section: Introductionmentioning

confidence: 91%

Section: Transfectionmentioning

confidence: 99%

Inhibition of Collagen XVI Expression Reduces Glioma Cell Invasiveness

Bauer¹,

Ratzinger²,

Wales³

et al. 2011

Cell Physiol Biochem

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“…However, the migration potential of glioblastoma cells on collagen type XVI remained unaffected. Collagen type XVI appears to play a supportive role for tumour specific remodelling of extracellular matrix indicated through de novo expression by glioblastoma cells (Senner et al, 2008). Novel data suggest that in glioblastoma tissue collagen XVI may impair the cell-cell interaction in favour of enhancement of invasion.…”

Section: Notementioning

confidence: 97%

“…It is synthezised by dermal fibroblasts, smooth muscle cells (Grässel et al, 1996), dermal dendrocytes and dendritic cells in the skin (Akagi et al, 2002), articular and costal chondrocytes (Kassner et al, 2003), endometrial stromal cells (Tierney et al, 2003), basal dermal and oral keratinocytes (Grässel et al, 1999), bone marrow derived mesenchymal stem cells (Grässel et al, 2009), neurons from the dorsal root ganglion (Hubert et al, 2007), glioblastoma/astrocytoma cells (Senner et al, 2008) and intestinal myofibroblasts (Ratzinger et al, 2010). Collagen type XVI is further expressed in the limbal stem/progenitor niche which comprises clusters of cells in the basal epithelium.…”

Section: Expressionmentioning

confidence: 99%

“…It is a substrate for adhesion and invasion of tumor cells, i.e. glioblastomas (Senner et al, 2008) and regeneration of connective tissues after neural injury (Hubert et al, 2007). In addition, it induces invasiveness of glioblastoma by altering the cell-matrix interaction and proliferative activity of oral squamous cell carcinoma by altering the cell cycle activity of the tumor cells .…”

Section: Functionmentioning

confidence: 99%

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COL16A1 (collagen, type XVI, alpha 1)

Grässel¹,

Bauer²

2012

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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Serum type XVI collagen is associated with colorectal cancer and ulcerative colitis indicating a pathological role in gastrointestinal disorders

et al. 2018

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Altered extracellular matrix (ECM) remodeling is an important part of the pathology of gastrointestinal (GI) disorders. In the intestine, type XVI collagen (col‐16) plays a role in pathogenesis by affecting ECM architecture and induce cell invasion. Measuring col‐16 in serum may therefore have biomarker potential in GI disorders such as colorectal cancer (CRC) and ulcerative colitis (UC). The aim of this study was to determine whether col‐16 can serve as a biomarker for altered ECM remodeling in patients with CRC and UC. A monoclonal antibody was raised against the C‐terminal end of col‐16 (PRO‐C16), and a competitive enzyme‐linked immunosorbent assay (ELISA) was developed and technically validated. Levels of PRO‐C16 were measured in serum from patients with CRC (before (n = 50) and 3 months after (n = 23) tumor resections), UC (n = 39) and healthy controls (n = 50). The PRO‐C16 ELISA was specific toward the C‐terminal of col‐16. PRO‐C16 was significantly elevated both in serum from patients with CRC (P = 0.0026) and UC (P < 0.0001) compared to controls. No difference was detected in levels of PRO‐C16 between patients with CRC at baseline and 3 months after tumor resections (P > 0.999). Levels of PRO‐C16 identified patients with a GI disorder with a positive predictive value of 0.9 and an odds ratio of 12 (95%CI = 4.5‐29.5, P < 0.0001). The newly developed assay detected significantly elevated levels of PRO‐C16 in serum from patients with GI disorders compared to controls suggesting its potential as a biomarker in this setting. Future studies are needed to validate these findings.

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Collagen XVI expression is upregulated in glioblastomas and promotes tumor cell adhesion

Cited by 51 publications

References 19 publications

Inhibition of Collagen XVI Expression Reduces Glioma Cell Invasiveness

Inhibition of Collagen XVI Expression Reduces Glioma Cell Invasiveness

COL16A1 (collagen, type XVI, alpha 1)

Serum type XVI collagen is associated with colorectal cancer and ulcerative colitis indicating a pathological role in gastrointestinal disorders

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