Cadherin‐7 interacts with melanoma inhibitory activity protein and negatively modulates melanoma cell migration

Winklmeier, Andreas; Contreras-Shannon, Verónica; Arndt, Stephanie; Melle, Christian; Bosserhoff, Anja‐Katrin

doi:10.1111/j.1349-7006.2008.01048.x

Cited by 22 publications

(21 citation statements)

References 24 publications

(34 reference statements)

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“…It was shown that CDH7 plays a role in tumor development of malignant melanoma cells by interacting with melanoma inhibitory activity protein (MIA) and migration melanoma cell [41]. …”

Section: Resultsmentioning

confidence: 99%

Pathway landscapes and epigenetic regulation in breast cancer and melanoma cell lines

Baroudi

Sala

Cinti

et al. 2014

Theor Biol Med Model

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BackgroundEpigenetic variation is a main regulation mechanism of gene expression in various cancer histotypes, and due to its reversibility, the potential impact in therapy can be very relevant.MethodsBased on a selected pair, breast cancer (BC) and melanoma, we conducted inference analysis in parallel on a few cell lines (MCF-7 for BC and A375 for melanoma). Starting from differential expression after treatment with a demethylating agent, the 5-Aza-2'-deoxycytidine (DAC), we provided pathway enrichment analysis and gene regulatory maps with cross-linked microRNAs and transcription factors.ResultsSeveral oncogenic signaling pathways altered upon DAC treatment were detected with significant enrichment. We represented the association between these cancers by depicting the landscape of common and specific variation affecting them.

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“…It was shown that CDH7 plays a role in tumor development of malignant melanoma cells by interacting with melanoma inhibitory activity protein (MIA) and migration melanoma cell [41]. …”

Section: Resultsmentioning

confidence: 99%

Pathway landscapes and epigenetic regulation in breast cancer and melanoma cell lines

Baroudi

Sala

Cinti

et al. 2014

Theor Biol Med Model

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“…The MIA protein, the secreted inhibitor of cell growth, prevents the attachment of melanoma cells to the extracellular matrix, thus promoting invasion and metastazing [32–34]. As opposed to the TYR gene promoter, the activity of the human MIA gene promoter correlates with melanoma progression [35].…”

Section: Promoters That Are Specifically Active In Melanocytesmentioning

confidence: 99%

Promoters with Cancer Cell-Specific Activity for Melanoma Gene Therapy

Pleshkan¹,

Alekseenko²,

Zinovyeva³

et al. 2011

Acta Naturae

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Melanoma is one of the most aggressive tumors. It develops from pigment-forming cells (melanocytes) and results in a high number of lethal outcomes. The use of genetic constructs with the ability to specifically kill melanoma cells, but not normal cells, might increase the lifespan of patients, as well as improve their quality of life. One of the methods to achieve a selective impact for therapeutic genes on cancer cells is to utilize a transcriptional control mechanism using promoters that are specifically activated only in cancerous cells. In this review, promoters of the genes that are preferentially expressed in melanoma cells are described. These promoters, and other highly melanoma-specific regulatory elements, reduce the unspecific expression of therapeutic genes in normal tissues. Moreover, cancer-specific promoters and their elements are advantageous for the development of universal anticancer drugs. Examples of the use of double promoters that have a high potential as instruments in cancer gene therapy are also given in this review.

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“…Recombinant MIA inhibits melanoma cell growth and cell attachment in vitro [16]. Subsequent studies revealed that MIA interacts with extracellular matrix components, laminin and fibronectin, as well as with cellular matrix receptors integrin α5, integrin α4 [17] and cadherin 7 [18]. …”

Section: Introductionmentioning

confidence: 99%

MIA is a potential biomarker for tumour load in neurofibromatosis type 1

Kolanczyk

Mautner

Kossler

et al. 2011

BMC Med

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BackgroundNeurofibromatosis type 1 (NF1) is a frequent genetic disease characterized by multiple benign tumours with increased risk for malignancy. There is currently no biomarker for tumour load in NF1 patients.MethodsIn situ hybridization and quantitative real-time polymerase reaction were applied to investigate expression of cartilage-specific genes in mice bearing conditional inactivation of NF1 in the developing limbs. These mice do not develop tumours but recapitulate aspects of NF1 bone dysplasia, including deregulation of cartilage differentiation. It has been recently shown that NF1 tumours require for their growth the master regulator of cartilage differentiation SOX9. We thus hypothesized that some of the cartilage-specific genes deregulated in an Nf1Prx1 mouse model might prove to be relevant biomarkers of NF1 tumours. We tested this hypothesis by analyzing expression of the SOX9 target gene product melanoma-inhibitory activity/cd-rap (MIA) in tumour and serum samples of NF1 patients.ResultsIncreased expression of Mia was found in Nf1-deficient cartilage in mice. In humans, MIA was expressed in all NF1-related tumours and its serum levels were significantly higher in NF1 patients than in healthy controls. Among NF1 patients, MIA serum levels were significantly higher in those with plexiform neurofibromas and in those with large number of cutaneous (> 1,000) or subcutaneous (> 100) neurofibromas than in patients without such tumours. Most notably, MIA serum levels correlated significantly with internal tumour burden.ConclusionsMIA is a potential serum biomarker of tumour load in NF1 patients which could be useful in following the disease course and monitoring the efficacy of therapies.

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Cadherin‐7 interacts with melanoma inhibitory activity protein and negatively modulates melanoma cell migration

Cited by 22 publications

References 24 publications

Pathway landscapes and epigenetic regulation in breast cancer and melanoma cell lines

Pathway landscapes and epigenetic regulation in breast cancer and melanoma cell lines

Promoters with Cancer Cell-Specific Activity for Melanoma Gene Therapy

MIA is a potential biomarker for tumour load in neurofibromatosis type 1

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