Hypermethylated APC in serous carcinoma based on a meta-analysis of ovarian cancer

Shen, Chunyan; Sheng, Qifang; Zhang, Xiaojie; Fu, Yuling; Zhu, Kemiao

doi:10.1186/s13048-016-0271-6

Cited by 12 publications

(9 citation statements)

References 36 publications

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“…Decreases in the expression of certain components of the destruction complex are frequently observed in EOC [61]. For example, several studies have reported significantly higher methylation rates in the promoter region of APC in EOC tumors when compared to benign ovarian tumors or normal ovarian tissue samples [62–64]. However, the mechanisms underlying the hypermethylation and suppression of APC in EOC are not clear.…”

Section: Introductionmentioning

confidence: 99%

Wnt/β-catenin signalling in ovarian cancer: Insights into its hyperactivation and function in tumorigenesis

et al. 2019

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Epithelial ovarian cancer (EOC) is the deadliest female malignancy. The Wnt/β-catenin pathway plays critical roles in regulating embryonic development and physiological processes. This pathway is tightly regulated to ensure its proper activity. In the absence of Wnt ligands, β-catenin is degraded by a destruction complex. When the pathway is stimulated by a Wnt ligand, β-catenin dissociates from the destruction complex and translocates into the nucleus where it interacts with TCF/LEF transcription factors to regulate target gene expression. Aberrant activation of this pathway, which leads to the hyperactivity of β-catenin, has been reported in ovarian cancer. Specifically, mutations of CTNNB1, AXIN, or APC, have been observed in the endometrioid and mucinous subtypes of EOC. In addition, upregulation of the ligands, abnormal activation of the receptors or intracellular mediators, disruption of the βcatenin destruction complex, inhibition of the association of β-catenin/E-cadherin on the cell membrane, and aberrant promotion of the β-catenin/TCF transcriptional activity, have all been reported in EOC, especially in the high grade serous subtype. Furthermore, several non-coding RNAs have been shown to regulate EOC development, in part, through the modulation of Wnt/β-catenin signalling. The Wnt/β-catenin pathway has been reported to promote cancer stem cell self-renewal, metastasis, and chemoresistance in all subtypes of EOC. Emerging evidence also suggests that the pathway induces ovarian tumor angiogenesis and immune evasion. Taken together, these studies demonstrate that the Wnt/β-catenin pathway plays critical roles in EOC development and is a strong candidate for the development of targeted therapies.

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Section: Introductionmentioning

confidence: 99%

Wnt/β-catenin signalling in ovarian cancer: Insights into its hyperactivation and function in tumorigenesis

et al. 2019

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“…However, the correlation of RASSF1A promoter methylation between ovarian cancer and LMP tumors remains to be evaluated. No correlation of methylated CDH1 and APC within the promoter between ovarian carcinoma and LMP tumors was reported by some studies [53, 54]. In our meta-analysis, one study reported that RASSF1A promoter methylation had higher frequency in ovarian cancer (23 patients) compared with LMP tumors (23 patients) [40].…”

Section: Discussionmentioning

confidence: 96%

Relationship between RAS Association Domain Family Protein 1A Promoter Methylation and the Clinicopathological Characteristics in Patients with Ovarian Cancer: A Systematic Meta-Analysis

Wang

Cui

Zhang

et al. 2017

Gynecol Obstet Invest

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Background: To investigate the relationship between RAS association domain family protein 1A (RASSF1A) promoter methylation and the clinical features, and the survival of ovarian cancer patients. Methods: A comprehensive literature search was conducted in the PubMed, Embase, EBSCO, and Cochrane Library databases. The overall ORs with their 95% CIs were calculated in this meta-analysis. Results: Finally 17 relevant publications with 1,108 ovarian cancer samples were available for the current meta-analysis. RASSF1A promoter methylation had a significantly higher level in ovarian cancer than in low malignant potential (LMP) tumors. No significant relationship was observed between RASSF1A promoter methylation and the clinicopathological characteristics in ovarian cancer. Two studies reported that RASSF1A promoter methylation was not correlated with the survival of patients with ovarian cancer. Conclusions: Our findings suggest that the use of RASSF1A promoter methylation could distinguish ovarian cancer and LMP tumors. RASSF1A promoter methylation may not be correlated with the clinical features and the survival of ovarian cancer patients. More studies with large sample sizes are essential in the future.

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“…Previous research has proven that ovarian cancer is a genetic disease, which depends on alteration of multi‐cancer genes and anti‐cancer genes, multi‐stages and multi‐pathways, involving a variety of oncogenes activation and anti‐oncogene inactivation . At the present, it is revealed that many genes and their protein products related to ovarian cancer have been explored . For example, APC promoter hypermethylation has been proved highly relevant to the occurrence of ovarian cancer .…”

Section: Introductionmentioning

confidence: 99%

A prognostic 11 genes expression model for ovarian cancer

Men¹,

Liu

Ren

2017

J of Cellular Biochemistry

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The symptoms of ovarian cancer at early stages are usually absent which makes the diagnosis in its early stages exceedingly difficult. Previous research has proven that ovarian cancer is a genetic disease, which depends on the alteration of multi-cancer related genes and anti-cancer genes, multi-stages and multi-pathways, involving a variety of oncogene activation and anti-oncogene inactivation. For a better understanding of the prognostic classification of ovarian cancer, gene expression profiles were used to analyze the prognostic factors of ovarian cancer, and the prognostic model was used to classify the ovarian cancer samples. The ovarian cancer samples data were downloaded from TCGA dataset. Rebust likelihood-based survival model was built to find the key genes that could function as prognostic markers. The samples were classified by unsupervised hierarchical clustering. Furthermore, Kaplan-Meier survival analysis was used to analyze the differences in the prognosis of the samples. The prognostic model was used to classify the samples, and then the best classification model was selected as the prognostic model of ovarian cancer. Finally, GEO datasets were used for external data validation. A total of 886 genes with influence on prognosis was obtained. Then genomic combinations of 11 genes were screened out by random sampling. Then the active number of influential factors was counted based on the expression level of featured genes. When the number of influencing factors is ≥7, the prognosis difference among these genes is the largest (P-value = 0.000775); and this was chosen as the final Classification model. To summary, a prognostic 11genes expression model was preliminarily built to classify the ovarian cancer samples.

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Hypermethylated APC in serous carcinoma based on a meta-analysis of ovarian cancer

Cited by 12 publications

References 36 publications

Wnt/β-catenin signalling in ovarian cancer: Insights into its hyperactivation and function in tumorigenesis

Wnt/β-catenin signalling in ovarian cancer: Insights into its hyperactivation and function in tumorigenesis

Relationship between RAS Association Domain Family Protein 1A Promoter Methylation and the Clinicopathological Characteristics in Patients with Ovarian Cancer: A Systematic Meta-Analysis

A prognostic 11 genes expression model for ovarian cancer

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