Secretory Type II Phospholipase A2 (PLA2G2A) expression status in colorectal carcinoma derived cell lines and in normal colonic mucosa

Praml, Christian; Amler, Lukas C.; Dihlmann, Susanne; L, Finke; Schlag, Peter M.; Schwab, Manfred

doi:10.1038/sj.onc.1202121

Cited by 33 publications

(26 citation statements)

References 17 publications

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“…With a single exception (Nimmrich et al, 1997), loss of Pla2g2a has not been observed in human colon cancer (Riggins et al, 1995;Praml et al, 1998;Dobbie et al, 1997;Spirio et al, 1996), although as noted by Dove et al (1994), Gould et al (1996a), andMacPhee et al (1995), one would not expect to observe LOH for a secreted factor that presumably acts non-cell autonomously within the mouse intestinal crypt.…”

Section: Pla2g2a Lipid Metabolism and Intestinal Cancermentioning

confidence: 93%

The Mom1AKR intestinal tumor resistance region consists of Pla2g2a and a locus distal to D4Mit64

et al. 2000

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The Mom1 (Modi®er of Min-1) region of distal chromosome 4 was identi®ed during a screen for polymorphic modi®ers of intestinal tumorigenesis in Apc Min/+ mice. Here, we demonstrate that the Mom1 AKR allele consists of two genetic components. These include the secretory phospholipase Pla2g2a, whose candidacy as a Mom1 resistance modi®er has now been tested with several transgenic lines. A second region, distal to Pla2g2a, has also been identi®ed using ®ne structure recombinants. Pla2g2a AKR transgenic mice demonstrate a modest resistance to tumorigenesis in the small intestine and a very robust resistance in the large intestine. Moreover, the tumor resistance in the colon of Pla2g2a AKR animals is dosage-dependent, a ®nding that is consistent with our observation that Pla2g2a is expressed in goblet cells. By contrast, mice carrying the distal Mom1 modi®er demonstrate a modest tumor resistance that is con®ned to the small intestine. Thus, the phenotypes of these two modi®er loci are complementary, both in their quantitative and regional eects. The additive eects and tight linkage of these modi®ers may have been necessary for the initial identi®cation of the Mom1 region. Oncogene (2000) 19, 3182 ± 3192.

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Section: Pla2g2a Lipid Metabolism and Intestinal Cancermentioning

confidence: 93%

The Mom1AKR intestinal tumor resistance region consists of Pla2g2a and a locus distal to D4Mit64

et al. 2000

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“…The RUNX3 gene is located on the short arm of human chromosome 1 at 1p36 , a region in which it is suggested that genes playing roles in maintenance of chromosome stability, suppression of tumorigenesis, control of apoptosis, and DNA methylation are located (reviewed by Di Vinci et al, 1998a, b). Indeed, deletions at 1p36 are common in colorectal cancers (Tanaka et al, 1993;Praml et al, 1995;Ogunbiyi et al, 1997;Di Vinci et al, 1998a, b), which suggests that the loss of genes in this region might be implicated in chromosome instability (Di Vinci et al, 1998b). It has also been reported that Runt domain transcription factors are important targets of TGF-b signaling.…”

Section: Discussionmentioning

confidence: 99%

Promoter hypermethylation downregulates RUNX3 gene expression in colorectal cancer cell lines

Kang

Shin

et al. 2004

Oncogene

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It was recently reported that RUNX3 gene expression is significantly downregulated in human gastric cancer cells due to hypermethylation of its promoter region or hemizygous deletion (Cell, 109, 2002). To verify the genetic alterations and methylation status of the RUNX3 gene in colorectal carcinogenesis, we analysed for mutations, loss of heterozygosity (LOH), and RUNX3 gene promoter hypermethylation, in 32 colorectal cancer cell lines. RT-PCR analysis showed undetectable or low RUNX3 expression in 16 cell lines, and no mutations were found in the RUNX3 gene by PCR-SSCP analysis. Of these 16 cell lines, hypermethylation of the RUNX3 promoter was confirmed in 12. The following observations were made: (i) RUNX3 was re-expressed after 5-aza-2 0 -deoxycytidine treatment, (ii) the RUNX3 promoter was found to be methylated by MS-PCR, and (iii) hypermethylation of the RUNX3 promoter was confirmed by direct sequencing analysis after sodium bisulfite modification in the above 12 cell lines. RUNX3 was neither methylated nor expressed in four cell lines. Of these four, microsatellite instability (MSI) at the RUNX3 locus was found in three, SNU-61 (D1S246), SNU-769A, and SNU-769B (D1S199). This study suggests that transcriptional repression of RUNX3 is caused by promoter hypermethylation of the RUNX3 CpG island in colorectal cancer cell lines, and the results of these experiments may contribute to an understanding of the role of RUNX3 inactivation in the pathogenesis of colorectal cancers.

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“…This chromosome location has been identi®ed by loss of heterozygosity studies as a site of a putative tumor suppressor gene or genes for breast carcinoma, colon carcinoma, neuroblastoma, non small cell lung carcinoma, melanoma, hepatocellular carcinoma, prostate, pancreatic endocrine tumors and Wilms' tumors (Nagai et al, 1995;Praml et al, 1995;Bieche et al, 1998;Martinsson et al, 1997;Ebrahimi et al, 1999;Gasparian et al, 1998;Chen et al, 1996;Boni et al, 1998;Williamson et al, 1997;Steenman et al, 1997;Sattler et al, 1999). However, we have not been unable to detect a mutation in the two TERE1 exons in 30 TCCs/matched normal PBLs except in the RT4 bladder tumor cell line.…”

Section: Discussionmentioning

confidence: 99%

Isolation and characterization of the TERE1 gene, a gene down-regulated in transitional cell carcinoma of the bladder

et al. 2001

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We have identi®ed a novel cDNA product designated transitional epithelial response gene (TERE1), which was localized to chromosome 1p36. The TERE1 transcript (1.5 and 3.5 kb) is present in most normal human tissues including urothelium, but was reduced or absent in the majority of muscle invasive TCC tumors (22 out of 29 cases). The open reading frame encodes a protein of 338 amino acids (MW 36.8 KD). This protein is 57% homologous to a Drosophila protein called heix. We have shown by Western blotting and immuno-histochemistry with a polyclonal antibody to a speci®c TERE1 peptide, reduced or absent staining in muscle invasive tumors. Transfection of a sense TERE1 construct resulted in an 80 ± 90% inhibition of cellular proliferation in two TCC cell lines and a lack of aneuploidy in the TERE1-transduced J82 cell line. These data suggest a potential role for this gene product in the progression of bladder cancer. Oncogene (2001) 20, 1042 ± 1051.

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Secretory Type II Phospholipase A2 (PLA2G2A) expression status in colorectal carcinoma derived cell lines and in normal colonic mucosa

Cited by 33 publications

References 17 publications

The Mom1AKR intestinal tumor resistance region consists of Pla2g2a and a locus distal to D4Mit64

The Mom1AKR intestinal tumor resistance region consists of Pla2g2a and a locus distal to D4Mit64

Promoter hypermethylation downregulates RUNX3 gene expression in colorectal cancer cell lines

Isolation and characterization of the TERE1 gene, a gene down-regulated in transitional cell carcinoma of the bladder

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