Mouse CD-RAP/MIA gene: Structure, chromosomal localization, and expression in cartilage and chondrosarcoma

Bosserhoff, Anja‐Katrin; Kondo, Seiji; Moser, Markus; Dietz, Uwe; Copeland, Neal G.; Gilbert, Debra J.; Jenkins, Nancy A.; Buettner, Reinhard; Sandell, Linda J.

doi:10.1002/(sici)1097-0177(199704)208:4<516::aid-aja7>3.0.co;2-l

Cited by 96 publications

(77 citation statements)

References 26 publications

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“…Homologues with more than 85% amino acid identity have been identified in mouse, rat, and cow (Bosserhoff et al, 1997c;Dietz and Sandell, 1996). MIA is highly and broadly expressed by chondrocytes during fetal chondrogenesis and in adult cartilaginous tissues, and it is believed to function as a regulatory molecule in cartilage formation (Bosserhoff et al, 1997c;Dietz and Sandell, 1996;Neame et al, 1999). Therefore, MIA is also known as cartilage-derived reti-noic acid-sensitive protein (CD-RAP) (Dietz and Sandell, 1996).…”

Section: Introductionmentioning

confidence: 99%

Identification and Characterization of an Inner Ear-Expressed Human Melanoma Inhibitory Activity (MIA)-like Gene (MIAL) with a Frequent Polymorphism That Abolishes Translation

et al. 2001

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To discover new cochlea-specific genes as candidate genes for nonsyndromic hearing impairment, we searched in The Institute of Genome Research database for expressed sequence tags isolated from the cochlea only. This led to the cloning and characterization of a human gene named melanoma inhibitory activity-like (MIAL; HGMW-approved symbol OTOR alias MIAL) gene. In situ hybridization revealed MIAL expression in a cell layer beneath the sensory epithelium of cochlea and vestibule of human fetal inner ear. No other human tissue, except fetal brain, showed expression of MIAL when analyzed by in situ hybridization or reverse transcription-polymerase chain reaction. The cDNA of the mouse homologue was also cloned and mapped about 80 cM from the top of mouse chromosome 2. In mouse, Mial was also expressed in the cochlea and the vestibule of the inner ear, as well as in brain, eye, limb, and ovary. Expression in mammalian cell cultures showed that MIAL is translated as an ϳ15-kDa polypeptide that is assembled into a covalently linked homodimer, modified by sulfation, and secreted from the cells via the Golgi apparatus. In the human MIAL gene, a frequent polymorphism was discovered in the translation initiation codon (ACG instead of ATG). Of 505 individuals, 48 (9.5%) were ATG/ ACG heterozygous and 1 (0.2%) was homozygous for ACG. No MIAL protein was synthesized in cells transfected with cDNA of the ACG allele. The inner earrestricted expression pattern and the existence of an inactive allele suggest that MIAL may contribute to inner-ear dysfunction in humans.

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Section: Introductionmentioning

confidence: 99%

Identification and Characterization of an Inner Ear-Expressed Human Melanoma Inhibitory Activity (MIA)-like Gene (MIAL) with a Frequent Polymorphism That Abolishes Translation

et al. 2001

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“…MIA has been characterized as a protein secreted by all primary and metastatic malignant melanoma and in addition by chondrosarcomas and many adenocarcinomas, including colorectal and breast cancer. 28,31,32 The MIA gene was independently cloned by differential display comparing differentiated and dedifferentiated chondrocytes and has been named cartilage-derived retinoic acid-sensitive protein (CD-RAP). 45 While MIA mediates the detachment of melanoma cells from extracellular matrix molecules such as fibronectin, 26 its expression in non-neoplastic tissues is only activated during the initiation of chondrogenesis throughout cartilage development indicating a highly selective expression pattern of the MIA gene.…”

Section: Discussionmentioning

confidence: 99%

“…45 While MIA mediates the detachment of melanoma cells from extracellular matrix molecules such as fibronectin, 26 its expression in non-neoplastic tissues is only activated during the initiation of chondrogenesis throughout cartilage development indicating a highly selective expression pattern of the MIA gene. 31,45 Two different variants, a full-length 1386 bp and a minimal 493 bp MIA promoter fragment were employed to drive selective gene expression. Since both fragments alone exhibited only weak transcriptional activity (data not shown), they were fused to four tandem copies of the enhancer of the murine tyrosinase gene.…”

Section: Discussionmentioning

confidence: 99%

“…[28][29][30] It has been shown that a fragment of approximately 1.4 kb 5 0 flanking DNA of the human gene conferred selective gene expression to melanoma cells, but not to melanocytes. 31 MIA activity is also detectable in chondrosarcomas, adenocarcinomas and chondrocytes. 28,31,32 In this study, gene regulatory elements from the tyrosinase and the MIA gene were combined to highly restrict HSVtk expression to melanoma cells and packed into recombinant AAV (rAAV) particles for efficient gene transfer.…”

mentioning

confidence: 95%

“…31 MIA activity is also detectable in chondrosarcomas, adenocarcinomas and chondrocytes. 28,31,32 In this study, gene regulatory elements from the tyrosinase and the MIA gene were combined to highly restrict HSVtk expression to melanoma cells and packed into recombinant AAV (rAAV) particles for efficient gene transfer. The results obtained demonstrated that infection with AAV mediated strong and highly selective suicide gene expression in vitro, and also the results in vivo may be an indicator for a stable transcriptional activity making them to a promising tool for tumor suicide gene therapy.…”

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confidence: 96%

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MIA (melanoma inhibitory activity) promoter mediated tissue-specific suicide gene therapy of malignant melanoma

Schoensiegel

Paschen

Sieger³

et al. 2004

Cancer Gene Ther

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Suicide gene therapy of malignant melanoma essentially requires efficient gene transfer and highly selective therapeutic gene expression. To achieve this, recombinant adeno-associated virus (rAAV) particles were constructed containing the tissue-specific promoter of the human melanoma inhibitory activity (hMIA) gene combined with four copies of the enhancer element of the murine tyrosinase gene. Three melanoma and one cervix carcinoma cell line were infected with rAAV particles carrying a reporter gene under control of the enhancer/hMIA promoter in order to determine transcriptional activity and specificity of this system. Viral particles containing the enhancer/hMIA promoter mediated reporter gene activity only in melanoma cells, whereas infection with a cytomegalovirus (CMV)-based promoter construct induced unspecific gene expression. Correspondingly, transient transduction with viral particles bearing the HSVtk gene under the control of the enhancer/MIA promoter elements followed by treatment with ganciclovir (GCV) resulted in growth inhibition only in melanoma cells, whereas the CMV promoter-based construct induced unspecific cytotoxicity. In vivo experiments in nude mice demonstrated that tumors originating from human melanoma cells disappeared after stable, but not transient transduction with vectors bearing the HSVtk gene under the control of the enhancer/hMIA promoter in response to GCV application. In face of higher transduction efficiency, these rAAV particles might therefore be a useful tool for suicide gene therapy of malignant melanoma.

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In situ expression patterns of melanoma-inhibiting activity (MIA) in melanomas and breast cancers

et al. 1999

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Elevated levels of melanoma‐inhibiting activity (MIA) were measured previously in the serum of patients with metastasized melanomas and in a subgroup of patients with advanced‐stage breast cancers. This study aimed therefore to visualize in situ expression patterns of MIA protein and mRNA in melanomas and breast cancers by means of immunohistochemistry, reverse transcription‐polymerase chain reaction (RT‐PCR), and in situ hybridization. Analysis of a panel of seven common melanocytic naevi, ten cutaneous melanomas, and 12 melanoma metastases detected high levels of both mRNA and protein in all melanomas and metastases, but only very low mRNA levels in three of seven naevi. Compared with the expression of pMel (HMB‐45), tyrosine, and S‐100 in these tumours, these results show that MIA provides a novel and sensitive marker for neoplastic melanocytes. Expression was not detected in other skin tumours including basal cell cancers and squamous cell cancers, nor in normal melanocytes and keratinocytes. MIA expression in adenocarcinomas was further studied in a panel of 20 specimens obtained from 16 advanced‐stage breast cancers and four metastases. Significant levels of mRNA were detected in 17 of the 20 specimens and low levels in the other three tumours. Immunostaining visualized specific protein expression in the tumour cells of all 20 cancer specimens. These investigations define for the first time in situ expression patterns of MIA in melanomas and breast cancers and suggest a much broader expression in malignant epithelial neoplasms than previously determined by serum studies. Copyright © 1999 John Wiley & Sons, Ltd.

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Mouse CD-RAP/MIA gene: Structure, chromosomal localization, and expression in cartilage and chondrosarcoma

Cited by 96 publications

References 26 publications

Identification and Characterization of an Inner Ear-Expressed Human Melanoma Inhibitory Activity (MIA)-like Gene (MIAL) with a Frequent Polymorphism That Abolishes Translation

Identification and Characterization of an Inner Ear-Expressed Human Melanoma Inhibitory Activity (MIA)-like Gene (MIAL) with a Frequent Polymorphism That Abolishes Translation

MIA (melanoma inhibitory activity) promoter mediated tissue-specific suicide gene therapy of malignant melanoma

In situ expression patterns of melanoma-inhibiting activity (MIA) in melanomas and breast cancers

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