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SPINK1 expression was associated with a shorter time to castration-resistant prostate cancer in metastatic prostate cancer in Japanese men.
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SPINK1 inhibition by shSPINK1 suppressed the development of lung adenocarcinoma and SPINK1 played a pro-tumor role by promoting cell proliferation and invasion.
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PRSS1 and SPINK1 mutations serve as genetic background for hereditary pancreatitis in Japan
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SPINK1 is both a targetable senescence-associated secretory phenotype factor and a novel noninvasive biomarker of therapeutically damaged tumor microenvironment.
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3 siblings with near identical clinical manifestations of early onset acute recurrent pancreatitis (ARP), all possessing the same heterozygous for serine protease inhibitor, Kazal type 1 (SPINK1) mutation c.55+1G>A.
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We demonstrate for the first time a significant decrease of SPINK1 levels after surgical decompression of pancreatic duct and a reduction of trypsin activity analysis after endoscopic decompression
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SPINK1 over expression is associated with prostate cancer specific mortality in at risk men with biochemical and clinical recurrence after prostatectomy
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Data show that alteration in beta-catenin expression, a core component of the CDH17/beta-catenin axis, in tumors affects serine peptidase inhibitor Kazal type 1 (SPINK1) serum levels in hepatocellular carcinoma (HCC) patients.
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Findings indicate that the serine protease inhibitor, Kazal type 1 (SPINK1) p.N34S allele may cause reduced SPINK1 expression.
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Having correlated our findings with current knowledge of SPINK1's role in exocrine pancreas pathophysiology, we propose that complete and partial functional losses of the SPINK1 gene are associated with quite distinct phenotypes, the former causing a new pediatric disease entity of severe infantile isolated exocrine pancreatic insufficiency (EPI) .
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results suggest that rs142703147:C>A, which disrupts a PTF1L-binding site within an evolutionarily conserved HNF1A-PTF1L cis-regulatory module located upstream of the SPINK1 promoter, contributes to the chronic pancreatitis risk haplotype.
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Studied mutations in cationic trypsinogen (PRSS1) and serine protease inhibitor Kazal type 1 (SPINK1) and their association with alcoholic chronic pancreatitis (ACP) and idiopathic chronic pancreatitis.
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Studies indicate that serine peptidase inhibitor Kazal type 1 (SPINK1) gene, particularly the N34S mutation, has a genetic association with the development of pancreatitis [Meta-analysis].
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association between SPINK1 p.N34S gene variation and chronic pancreatitis [review, meta-analysis]
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We present the case of a child with a homozygous mutation N34S in the SPINK1 gene, leading to acute recurrent pancreatitis and ultimately to chronic pancreatitis
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Used in silico splicing prediction programs to prioritize SPINK1 intronic variants for further quantitative RT-PCR analysis the non-pathological c.194 + 13T > G variant was predicted by different programs to generate a new & viable donor splice site, the prediction scores being comparable to those for the physiological c.194 + 2T donor splice site & even higher than those for the physiological c.87 + 1G donor splice site.
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Gene mutations were present in PRSS1 in 26 patients with acute recurrent and chronic pancreatitis, SPINK1 in 23, CTRC in 3, and CPA1 in 5. In the 31 patients with mutations in SPINK1, CTRC, or CPA1, 16 (51.6%) had homozygous or heterozygous mutations with other mutations.
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SPINK1 can associate with EGFR to promote the expression of cell proliferation-related and anti-apoptosis-related genes/proteins; inhibit the expression of pro-apoptosis-related genes/proteins via p38, ERK, and JNK pathways; and consequently promote the proliferation of BRL-3A cells.
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The present study demonstrates for the first time that both fibroblast-derived and recombinant IL-6 induces SPINK1 expression and secretion in in colorectal adenocarcinoma.
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Absolute exclusivity between SPINK1 overexpression and homozygous PTEN deletion in localized PCA.
