@article{TCR7351,
author = {Govinda Lenka and Mong-Hsun Tsai and Jen-Hao Hsiao and Liang-Chuan Lai and Eric Y. Chuang},
title = {Overexpression of methylation-driven DCC suppresses proliferation of lung cancer cells},
journal = {Translational Cancer Research},
volume = {5},
number = {2},
year = {2016},
keywords = {},
abstract = {Background: DNA methylation is an epigenetic marker associated with regulation of gene expression and gene silencing. The active role of DNA methylation has been thoroughly studied in a number of cancer types. The deleted in colorectal carcinoma (DCC) gene, located at chromosome 18q21, plays an important role as a tumor suppressor and is associated with hypermethylation in head and neck squamous cell carcinoma. However, the methylation patterns and functional significance of DCC in lung cancer are still not known.
Methods: RT-PCR was used to examine the endogenous expression levels of DCC in two lung cancer cell lines (A549, H1299) and their normal counterpart (Beas-2B). The demethylating agent, 5-aza-2'-deoxycytidine (5-aza), was used to examine the role of methylation in regulating expression of DCC in lung cancer cell lines. DCC was also overexpressed to evaluate its role in proliferation and colony formation. Finally, the gene expression signature of public dataset GSE68456 was used to elucidate the prognostic roles of DCC in lung adenocarcinoma patients.
Results: Endogenous expression of DCC was significantly decreased in lung cancer compared to the normal cells (P},
issn = {2219-6803}, url = {https://tcr.amegroups.org/article/view/7351}
}