Entrez Gene

General information | Expression | Regulation | Mutation | Interaction

Basic Information
Gene ID	5276
Name	SERPINI2
Synonymous	MEPI\|PANCPIN\|PI14\|TSA2004;serpin peptidase inhibitor, clade I (pancpin), member 2;SERPINI2;serpin peptidase inhibitor, clade I (pancpin), member 2
Definition	PI-14\|myoepithelium-derived serine protease inhibitor\|pancreas-specific protein TSA2004\|peptidase inhibitor 14\|protease inhibitor 14\|serine (or cysteine) proteinase inhibitor, clade I (neuroserpin), member 2\|serine (or cysteine) proteinase inhibitor, clad
Position	3q26
Gene type	protein-coding
Source	Count: 2; TAG,Generif
Sentence	Abstract
Serpini2 was initially identified and implicated as a potential tumor suppressor gene because it was downregulated in pancreatic cancer cell lines when compared to normal pancreas.	By means of the differential display method, we isolated a novel human gene that is expressed specifically in pancreas. The cDNA, designated "pancpin," contained an open reading frame of 1,215 nucleotides encoding a 405 amino acid protein, showing a high degree of similarity to serine protease inhibitors belonging to the serpin superfamily. To investigate its possible role in pancreatic carcinogenesis, we looked for genetic alterations of this gene in pancreatic cancer cell lines and primary pancreatic cancer tissues. expression of pancpin was barely detectable in any of the four pancreatic cancer cell lines examined, and very weak also in 10 of 13 pancreatic cancer tissues. A somatic missense mutation at codon 221 was found in two of 16 primary pancreatic cancers. These findings indicate that down-regulation of pancpin expression may play a significant role in development or progression of pancreatic cancer.
Notable genes include hypoxia and tumor growth regulator Loxl2 [26] and tumor suppressor Serpini2.	ABSTRACT: BACKGROUND: Malignant ovarian disease is characterised by high rates of mortality due to high rates of recurrent chemoresistant disease. Anecdotal evidence indicates this may be due to chemoresistant properties of cancer stem cells (CSCs). However, our understanding of the role of CSCs in recurrent ovarian disease remains sparse. In this study we used gene microarrays and meta-analysis of our previously published microRNA (miRNA) data to assess the involvement of cancer stemness signatures in recurrent ovarian disease. METHODS: Microarray analysis was used to characterise early regulation events in an embryonal carcinoma (EC) model of cancer stemness. This was then compared to our previously published microarray data from a study of primary versus recurrent ovarian disease. In parallel, meta-analysis was used to identify cancer stemness miRNA signatures in tumor patient samples. RESULTS: Microarray analysis demonstrated a 90% difference between gene expression events involved in early regulation of differentiation in murine EC (mEC) and embryonic stem (mES) cells. This contrasts the known parallels between mEC and mES cells in the undifferentiated and well-differentiated states. Genelist comparisons identified a cancer stemness signature set of genes in primary versus recurrent data, a subset of which are known p53-p21 regulators. This signature is present in primary and recurrent or in primary alone but essentially never in recurrent tumors specifically. Meta-analysis of miRNA expression showed a much stronger cancer stemness signature within tumor samples. This miRNA signature again related to p53-p21 regulation and was expressed prominently in recurrent tumors. Our data indicate that the regulation of p53-p21 in ovarian cancer involves, at least partially, a cancer stemness component. CONCLUSION: We present a p53-p21 cancer stemness signature model for ovarian cancer. We propose that this may, at least partially, differentially regulate the p53-p21 mechanism in ovarian disease. Targeting CSCs within ovarian cancer represents a potential therapeutic avenue.