Search engine for discovering works of Art, research articles, and books related to Art and Culture
ShareThis
Javascript must be enabled to continue!

Aberrant OCIAD2 demethylation in lung adenocarcinoma is associated with outcome

View through CrossRef
AbstractOverexpression of OCIAD2 in lung adenocarcinoma has already been reported in several research articles, but the molecular mechanism involved remains unknown. Promoter CpG methylation is a representative form of epigenetic gene regulation, and a considerable number of tumor suppressor genes show hypermethylation in many cancers. In contrast, promoter CpG hypomethylation causes oncogene overexpression, resulting in carcinogenesis and malignant progression. In the present study, we investigated the CpG methylation and expression status of OCIAD2 using tumor tissues and adjacent normal tissues from seven cases of lung adenocarcinoma. We also examined the relationship between CpG methylation status and outcome in 58 patients with adenocarcinoma. Pyrosequencing showed that CpG sites in OCIAD2 promoter regions were more frequently demethylated in tumor tissues than in adjacent normal tissues, and reverse transcription‐quantitative polymerase chain reaction revealed overexpression of OCIAD2 in lung adenocarcinoma. There was a correlation between OCIAD2 CpG demethylation and the level of mRNA expression, and statistical analysis showed that CpG hypomethylation of OCIAD2 was associated with poor outcomes. Our results suggest that overexpression of OCIAD2 might be caused mainly by CpG hypomethylation and that OCIAD2 methylation status might be a useful prognostic indicator in lung adenocarcinoma.
Title: Aberrant OCIAD2 demethylation in lung adenocarcinoma is associated with outcome
Description:
AbstractOverexpression of OCIAD2 in lung adenocarcinoma has already been reported in several research articles, but the molecular mechanism involved remains unknown.
Promoter CpG methylation is a representative form of epigenetic gene regulation, and a considerable number of tumor suppressor genes show hypermethylation in many cancers.
In contrast, promoter CpG hypomethylation causes oncogene overexpression, resulting in carcinogenesis and malignant progression.
In the present study, we investigated the CpG methylation and expression status of OCIAD2 using tumor tissues and adjacent normal tissues from seven cases of lung adenocarcinoma.
We also examined the relationship between CpG methylation status and outcome in 58 patients with adenocarcinoma.
Pyrosequencing showed that CpG sites in OCIAD2 promoter regions were more frequently demethylated in tumor tissues than in adjacent normal tissues, and reverse transcription‐quantitative polymerase chain reaction revealed overexpression of OCIAD2 in lung adenocarcinoma.
There was a correlation between OCIAD2 CpG demethylation and the level of mRNA expression, and statistical analysis showed that CpG hypomethylation of OCIAD2 was associated with poor outcomes.
Our results suggest that overexpression of OCIAD2 might be caused mainly by CpG hypomethylation and that OCIAD2 methylation status might be a useful prognostic indicator in lung adenocarcinoma.

Related Results

Minimally Invasive Thoracoscopic Surgery of Lung Adenocarcinoma in Old Age People
Minimally Invasive Thoracoscopic Surgery of Lung Adenocarcinoma in Old Age People
Background: Lung cancer is the most frequent human malignancy and the principal cause of cancer-related death worldwide. Adenocarcinoma is now the main histologic type, accounting ...
USP4 promotes proliferation and metastasis in human lung adenocarcinoma
USP4 promotes proliferation and metastasis in human lung adenocarcinoma
Abstract Objective Research the expression of USP4 in lung adenocarcinoma and its correlation with clinicopathological features and prognosis analysis, to explore the inva...
Experience Sharing in Pathological Diagnosis of Early Adenocarcinoma of the Lung
Experience Sharing in Pathological Diagnosis of Early Adenocarcinoma of the Lung
Background: In daily work, there are still many pathologists who have difficulty handling the diagnosis of atypical adenomatous hyperplasia, adenocarcinoma in situ, minimally invas...
Abstract 1657: Genome-wide association study of lung cancer: Variation in TP63 gene confers the risk of lung adenocarcinoma
Abstract 1657: Genome-wide association study of lung cancer: Variation in TP63 gene confers the risk of lung adenocarcinoma
Abstract Lung cancer is the most common cause of death from cancer worldwide, and its incidence is increasing in East Asian and Western countries. Lung cancer compri...
Microwave Ablation with or Without Chemotherapy in Management of Non-Small Cell Lung Cancer: A Systematic Review
Microwave Ablation with or Without Chemotherapy in Management of Non-Small Cell Lung Cancer: A Systematic Review
Abstract Introduction  Microwave ablation (MWA) has emerged as a minimally invasive treatment for patients with inoperable non-small cell lung cancer (NSCLC). However, whether it i...
The identification of novel biomarkers offers potential avenues for therapeutic interventions in lung adenocarcinoma
The identification of novel biomarkers offers potential avenues for therapeutic interventions in lung adenocarcinoma
Abstract Background: Lung cancer stands as a prominent contributor to cancer-related fatalities, with lung adenocarcinoma emerging as one of its primary histological subtyp...
JAK2 variations and functions in lung adenocarcinoma.
JAK2 variations and functions in lung adenocarcinoma.
e23181 Background: Lung cancer ranks as the first most common cancer and the first leading cause of cancer-related death in China and worldwide. Due to the difficulty in early dia...
Abstract 1769: The clinical outcome of stage I lung adenocarcinoma patients with or without activating EGFR mutation
Abstract 1769: The clinical outcome of stage I lung adenocarcinoma patients with or without activating EGFR mutation
Abstract Purpose: Advanced stage lung adenocarcinoma patients with activating EGFR mutation have better survival result after EGFR tyrosine kinase inhibitor develope...

Back to Top