Inhibition of Collagen XVI Expression Reduces Glioma Cell Invasiveness

Bauer, Robert; Ratzinger, Sabine; Wales, Lynn; Bosserhoff, Anja‐Katrin; Senner, Volker; Grifka, Joachim; Grässel, Susanne

doi:10.1159/000327947

Cited by 39 publications

(27 citation statements)

References 39 publications

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“…These levels were elevated in 60% of lung and 70% of colon cancers 57 . Kindlin-1 was also found to be associated with the pathology of glioma 58 . Kindlin-1 mRNA also was highly expressed in the pancreatic cancer cell lines and pancreatic cancer tissue 59 .…”

Section: Association Of Kindlins With Cancermentioning

confidence: 92%

Of Kindlins and Cancer

Plow

Das

Białkowska

et al. 2016

Discoveries (Craiova)

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Kindlins are 4.1-ezrin-ridixin-moesin (FERM) domain containing proteins. There are three kindlins in mammals, which share high sequence identity. Kindlin-1 is expressed primarily in epithelial cells, kindlin-2 is widely distributed and is particularly abundant in adherent cells, and kindlin-3 is expressed primarily in hematopoietic cells. These distributions are not exclusive; some cells express multiple kindlins, and transformed cells often exhibit aberrant expression, both in the isoforms and the levels of kindlins. Great interest in the kindlins has emerged from the recognition that they play major roles in controlling integrin function. In vitro studies, in vivo studies of mice deficient in kindlins, and studies of patients with genetic deficiencies of kindlins have clearly established that they regulate the capacity of integrins to mediate their functions. Kindlins are adaptor proteins; their function emanate from their interaction with binding partners, including the cytoplasmic tails of integrins and components of the actin cytoskeleton. The purpose of this review is to provide a brief overview of kindlin structure and function, a consideration of their binding partners, and then to focus on the relationship of each kindlin family member with cancer. In view of many correlations of kindlin expression levels and neoplasia and the known association of integrins with tumor progression and metastasis, we consider whether regulation of kindlins or their function would be attractive targets for treatment of cancer.

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Section: Association Of Kindlins With Cancermentioning

confidence: 92%

Of Kindlins and Cancer

Plow

Das

Białkowska

et al. 2016

Discoveries (Craiova)

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“…In normal oral epithelium as in the dermis, collagen XVI is predominantly located at the dermal-epidermal junction [8], [16]. Collagen XVI is involved in dermal architecture by interacting with integrins alpha1beta1, alpha2beta1 and the microfibrillar apparatus [8], [20].…”

Section: Discussionmentioning

confidence: 99%

“…It is not only produced by dermal fibroblasts but also by smooth muscle cells [9], dermal dendrocytes [10], articular and costal chondrocytes [7], endometrial stromal cells [11], basal dermal and oral keratinocytes [8], [12], [15], neurons from the dorsal root ganglion [13] and glioblastoma / astrocytoma cells [14]. Recent studies have shown, that collagen XVI is implicated in the development of glioblastoma and OSCC, in which it is overexpressed during tumor progression and influences cell cycle progression [12], [14]–[16].…”

Section: Introductionmentioning

confidence: 99%

Collagen XVI Induces Expression of MMP9 via Modulation of AP-1 Transcription Factors and Facilitates Invasion of Oral Squamous Cell Carcinoma

et al. 2014

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Collagen XVI belongs to the family of fibril-associated collagens with interrupted triple helices (FACIT). It is overexpressed during the progression of oral squamous cell carcinoma (OSCC). The present data show a strong collagen XVI-dependent induction of MMP9 and an increase in OSCC cell invasion. We found activated integrin-linked kinase (ILK) in a complex with kindlin-1 and activation of protein kinase B (PKB/Akt) to be responsible for MMP9 induction. Inhibition of the formation of focal adhesions reduced MMP9 expression. Moreover, collagen XVI overexpressing OSCC cell clones (COLXVI cell clones) transfected with vectors containing different MMP9 promoter fragments adjacent to a luciferase reporter revealed an increase in luciferase signal dependent on AP-1 binding sites. Deletion of the AP-1 binding site 98 bp upstream of the reported transcription start site and inhibition of AP-1 with Tanshinone IIA resulted in decreased MMP9 expression. The AP-1 subunit JunB showed differential expression between COLXVI cell clones and mock control cells. Additionally, mass spectrometric analysis of immunoprecipitates revealed that c-Fos interacted strongly with dyskerin in COLXVI cell clones compared to mock controls.

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“…The expression of several extracellular matrix and collagen genes has been related to invasion and survival in some other tumors. [47][48][49] The recognition of a desmoplastic response to cancer has long been recognized, [50][51][52] and the role of tumor-associated fibroblasts in the growth and development of cancer is a topic of recent research. 36,46,[53][54][55][56] The use of the AF gene set in the current study raises the question of the contribution of the stroma to the gene expression pattern and biology of the tumor.…”

Section: Discussionmentioning

confidence: 99%

Gene expression identifies heterogeneity of metastatic propensity in high‐grade soft tissue sarcomas

Skubitz

Francis

Skubitz

et al. 2012

Cancer

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BACKGROUND: Metastatic propensity of soft tissue sarcoma (STS) is heterogeneous and may be determined by gene expression patterns that do not correlate well with morphology. The authors have reported gene expression patterns that distinguish 2 broad classes of clear cell renal carcinoma (ccRCC-gene set), and other patterns that can distinguish heterogeneity of serous ovarian carcinoma (OVCA-gene set) and aggressive fibromatosis (AF-gene set); however, clinical follow-up data were not available for these samples. METHODS: In the current study, gene expression patterns in 73 samples of high-grade STS were examined using spotted cDNA microarray slides that contained 16,000 unique UniGene clusters. Approximately 50% of the genes present in the ccRCC-, OVCA-, and AF-gene sets were also represented in the data from this chip set, and these were combined to form a composite gene set of 278 probes. RESULTS: Hierarchical clustering using this composite gene set suggested the existence of subsets of the STS samples. Analysis revealed differences in the time to development of metastatic disease between the clusters defined by the first branch point of the clustering dendrogram (P ¼ .005), and also among the 4 different clusters defined by the second branch points (P ¼ .001). CONCLUSIONS: This approach suggests the existence of >2 subsets of high-grade pleomorphic STS, each with distinct clinical behavior. A composite gene set such as that described here may be useful to stratify STS in clinical trials, and may be of practical utility in patient management. Cancer 2012;118:4235-43.

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Inhibition of Collagen XVI Expression Reduces Glioma Cell Invasiveness

Cited by 39 publications

References 39 publications

Of Kindlins and Cancer

Of Kindlins and Cancer

Collagen XVI Induces Expression of MMP9 via Modulation of AP-1 Transcription Factors and Facilitates Invasion of Oral Squamous Cell Carcinoma

Gene expression identifies heterogeneity of metastatic propensity in high‐grade soft tissue sarcomas

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