Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The differential display technique was used to identify mRNAs differentially expressed in human melanoma cell lines with different metastatic capacity. We report the isolation of nine different clones, of which four were uniquely expressed in the highly metastatic human melanoma cell line MV3, whereas the other five clones were uniquely expressed in the poorly metastatic human melanoma cell line 530. The differences in expression identified by differential mRNA display were confirmed by Northern blot analyses. DNA sequencing followed by computer search analyses indicated that of the nine differentially expressed clones, five represented novel gene products. The other four were histocompatibility antigen HLA-DR, laminin B2, melanoma inhibitory activity (MIA), and tissue inhibitor of metalloproteinases 3. MIA was also identified in RNA from human melanoma metastasis lesions in a comparison by differential display with pooled human nevi. Northern blot analysis confirmed MIA mRNA expression in nonmetastasizing melanoma cell lines and in melanoma metastasis lesions, while expression was absent in highly metastasizing cell lines and pretumor stages. In the 11 metastasis lesions examined, MIA mRNA expression was apparently inversely correlated with pigmentation.
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PMID:Identification of melanoma inhibitory activity and other differentially expressed messenger RNAs in human melanoma cell lines with different metastatic capacity by messenger RNA differential display. 852 20

The protein melanoma inhibitory activity (MIA) is known to be expressed in melanoma and to support melanoma progression. Interestingly, previous studies also observed the expression of MIA in nevi. Concentrating on these findings, we revealed that MIA expression is correlated with a senescent state in melanocytes. Induction of replicative or oncogene-induced senescence resulted in increased MIA expression in vitro. Notably, MIA knockdown in senescent melanocytes reduced the percentage of senescence-associated beta-Gal-positive cells and enhanced proliferation. Using the melanoma mouse model Tg(Grm1), MIA-deficient mice supported the impact of MIA on senescence by showing a significantly earlier tumor onset compared to controls. In melanocytes, MIA knockdown led to a downregulation of the cell cycle inhibitor p21 in vitro and in vivo. In contrast, after induction of hTERT in human melanoma cells, p21 regulation by MIA was lost. In summary, our data show for the first time that MIA is a regulator of cellular senescence in human and murine melanocytes.
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PMID:Role of melanoma inhibitory activity in melanocyte senescence. 3117 72