Decreased expression of the Id3 gene at 1p36.1 in ovarian adenocarcinomas

Arnold, Jeremy M.; Mok, Samuel C.; Purdie, David M.; Chenevix-Trench, Georgia

doi:10.1054/bjoc.2000.1620

Cited by 30 publications

(32 citation statements)

References 37 publications

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“…19 In this study, Id-3 staining was not significantly different between nodular hyperplasia and lowgrade prostate cancer (Figure 3c). However, we observed a significant decrease in expression of Id-3 in high-grade prostate cancer as compared to low-grade prostate cancer (Figure 3c).…”

Section: Discussionmentioning

confidence: 46%

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Id proteins expression in prostate cancer: high-level expression of Id-4 in primary prostate cancer is associated with development of metastases

et al. 2006

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A major cause of treatment failure for prostate cancer is the development of androgen-independent metastatic disease. Id protein family, a group of basic helix-loop-helix transcription factors, has been shown to be involved in carcinogenesis and a prognostic marker in several types of human cancers. In this study, we examined the expressions of four Id proteins, Id-1, -2, -3 and -4, in 125 clinical prostate cancer specimens as well as 40 nodular hyperplasia specimens by immunohistochemistry. The expressions of Id proteins were correlated with Gleason grading and metastatic progress of the tumors. We found that Id proteins were dysregulated in prostate cancer. Id-1 and -2 expressions were elevated while Id-3 and -4 expressions were reduced in prostate cancers compared to nodular hyperplasia. Cytoplasmic staining of Id-1 (P ¼ 0.013) and nuclear staining of Id-2 (P ¼ 0.001) and Id-4 (Po0.001) were positively correlated with Gleason score. The results indicate that these Id proteins may play a positive role in the development of prostate cancer. In contrast, Id-3 might have an inverse relationship with prostate neoplastic transformation (P ¼ 0.002) and cancer progression (P ¼ 0.022). We found that Id-4 nuclear overexpression in the primary prostate cancers significantly increased the risks to the development of metastasis in the patients (odds ratio ¼ 3.215, 95% confidence interval ¼ 1.150-8.987, P ¼ 0.026). Our results suggest that in prostate cancer patients, differential Id proteins expressions may be a useful marker for poor prognosis, and Id-4 may be a potential prognostic marker for distant metastasis.

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Section: Discussionmentioning

confidence: 46%

“…Id-3 expression was reduced in ovarian cancer. 19 These results suggest that the expression of different Id proteins in different types of cancer could be used as prognostic markers of cancers.…”

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confidence: 93%

Id proteins expression in prostate cancer: high-level expression of Id-4 in primary prostate cancer is associated with development of metastases

et al. 2006

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“…Transgene expression of ID1 and ID2 in mice has resulted in tumor formation in the intestinal epithelium and lymphoid organs, respectively (Wice and Gordon 1998; Morrow et al, 1999). Expression of ID3 has been more variable with studies reporting both upregulation (Wilson et al, 2001;Vandeputte et al, 2002) and downregulation (Arnold et al, 2001;Deleu et al, 2002) in different tumor types. Little is known, however, about the expression, regulation and potential roles of ID4 in the carcinogenic process.…”

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confidence: 99%

Downregulation of ID4 by promoter hypermethylation in gastric adenocarcinoma

et al. 2003

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Promoter hypermethylation has become apparent as a common mechanism of gene silencing in cancer. Based on our published microarray expression data, we noticed a prominent downregulation of ID4 in gastric adenocarcinoma. The dense 5 0 CpG island covering the previously mapped upstream promoter of ID4 has prompted us to relate its downregulation to promoter hypermethylation. ID proteins are distinct members in the helix-loop-helix family of transcriptional regulators, which modulate various key developmental processes. Emerging data have suggested the involvement of ID genes in tumorigenesis. In this study using bisulfite genomic sequencing, we have found hypermethylation of ID4 promoter in most gastric cancer cell lines and 30% of primary tumors. This correlated with decreased level of ID4 expression. Restoration of ID4 expression in various gastric cancer cell lines was achieved by treatment with the DNA methyltransferase inhibitor 5-aza-2 0 -deoxycytidine, which at times required the synergistic action of the histone deacetylase inhibitor trichostatin A, but not with trichostatin A alone. Re-expression was accompanied by the corresponding ID4 promoter demethylation. Furthermore, we have found significant association of ID4 promoter methylation with hMLH1 promoter methylation (P ¼ 0.008) and microsatellite instability (P ¼ 0.006). Overall, our results have shown that transcriptional silencing of ID4 is related to the aberrant methylation of its promoter in gastric cancer. The significant association of ID4 and hMLH1 promoter hypermethylation suggested that ID4 may also be among the genes being targeted in the CpG island methylator phenotype tumorigenic pathway.

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“…We previously conducted a screen for genes aberrantly expressed in three ovarian adenocarcinoma cell lines compared to an immortalised HOSE using a human cDNA array containing 588 known genes (Arnold et al, 2001a). This showed that expression of CCL2 is greatly reduced in ovarian cancer cell lines.…”

Section: Ccl2 Expression Analysis In Ovarian Adenocarcinoma Cell Linesmentioning

confidence: 99%

“…Using cDNA array screening of normal OSE cells and ovarian cancer cell lines, we previously identified CCL2 as a gene whose expression is downregulated or lost in ovarian cancer cell lines (Arnold et al, 2001a). In this report, we describe the characterisation of CCL2 expression in a larger panel of ovarian cancer cell lines and primary tumours and mutation analysis of the CCL2 gene in primary ovarian adenocarcinomas.…”

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confidence: 93%

Reduced expression of chemokine (C-C motif) ligand-2 (CCL2) in ovarian adenocarcinoma

et al. 2005

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Chemokine (C-C motif) ligand-2 (CCL2) is a chemoattractant and activator of macrophages and is a key determinant of the macrophage infiltrate into tumours. We demonstrate here that CCL2 is expressed in normal human ovarian surface epithelium (HOSE) cells and is silenced in most ovarian cancer cell lines, and silenced or downregulated in the majority of primary ovarian adenocarcinomas. Analysis of the CCL2 locus at 17q11.2 -q12 showed loss of heterozygosity (LOH) in 70% of primary tumours, and this was significantly more common in tumours of advanced stage or grade. However, we did not detect any mutations in the CCL2 coding sequence in 94 primary ovarian adenocarcinomas. These data support the hypothesis that CCL2 may play a role in the pathobiology of ovarian cancers, but additional studies will be required to evaluate this possibility.

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Decreased expression of the Id3 gene at 1p36.1 in ovarian adenocarcinomas

Cited by 30 publications

References 37 publications

Id proteins expression in prostate cancer: high-level expression of Id-4 in primary prostate cancer is associated with development of metastases

Id proteins expression in prostate cancer: high-level expression of Id-4 in primary prostate cancer is associated with development of metastases

Downregulation of ID4 by promoter hypermethylation in gastric adenocarcinoma

Reduced expression of chemokine (C-C motif) ligand-2 (CCL2) in ovarian adenocarcinoma

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