SERPINB5

SERPINB5

A gene on chromosome 18q21.3 that encodes a member of the serine protease inhibitor (serpin) family that acts as a tumour suppressor by blocking the growth, invasion and metastatic properties of mammary tumours. SERPINB5 does not undergo the S (stressed) to R (relaxed) conformational transition characteristic of active serpins; it has no serine protease inhibitory activity.
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132 With oligonucleotide microarray technologies, 2 additional genes, S100P (chromosome arm 4p) and SERPINB5 (chromosome arm 18q, encoding maspin), have been identified as being hypomethylated and are overexpressed.
3 E1B 19 kDa interacting protein 3 miR9-1 MicroRNA 9-1 Hypermethylation 1q22 SERPINB5 Serpin peptidase Hypomethylation 18q21.
have reported that the SERPINB5 gene, coding for maspin, is hypomethylated in placental tissues and hypermethylated in maternal blood cells (11).
Since the development of the SERPINB5 marker, many other fetal epigenetic markers suitable for detection in maternal plasma have been described, including the RASSFIA gene on chromosome 3 (21, 22) and numerous markers on chromosome 21 (23, 24).
For DNA methylation markers, the first demonstration is the use of hypomethylated SERPINB5 sequences as a fetus-specific target on chromosome 18 (11).
The genes that were more highly expressed in carcinomas treated with androgen ablation agents included those encoding AR and steroid biosynthetic enzymes, as well as a suite of genes that have been previously shown to be targets of AR or have been implicated as being regulated by it, including the gene encoding PSA (kallikrein-related peptidase 3), KLK3, and KLK2, as well as DBI, FASN, IL6, SERPINB5, TGFBR3, TMPRSS2, TUBA1, HOXC6, TRG ,and FOLH1.
Subsequently, we discovered the SERPINB5 [5] gene [serpin peptidase inhibitor, clade B (ovalbumin), member 5; also known as maspin] to be hypomethylated in the placenta but completely methylated in maternal blood cells.
To detect hypomethylated placental SERPINB5 in an excess background of hypommethylated SERPINB5 of maternal origin in maternal plasma, the use of bisulfite treatment was reported (19, 20).
If the same approach were to be applied to the detection of the placenta-derived hypomethylated SERPINB5 molecules, an endonuclease that exhibits an opposite action to the methylation-sensitive restriction endonucleases described above would be needed.
The specificity of the stem-loop primers to detect enzyme-digested DNA fragments was evaluated by genotyping of the SERPINB5 -156 single-base variation of placental-maternal DNA mixtures with different feto-maternal genotypes (15).
Lo demonstrated that the tumor suppressor gene RASS-F1A exhibits a pattern of methylation which is reverse to that of SERPINB5, namely hypermethylated in the placenta but hypomethylated in maternal blood cells.