Literature DB >> 20862745

Promoter methylation of the RGC32 gene in nonsmall cell lung cancer.

Dong Sun Kim1, Ji Yun Lee, Su Man Lee, Jin Eun Choi, Sukki Cho, Jae Yong Park.   

Abstract

BACKGROUND: Lung cancer is the leading cause of cancer-related deaths worldwide. Epigenetic inactivation of certain genes by aberrant promoter methylation is recognized as a crucial component in the initiation and progression of lung cancer. Response gene to complement 32 (RGC32) has been identified as a cell cycle regulator induced by activation of complements; however, its role in carcinogenesis is still controversial.
METHODS: The authors examined the methylation status in the promoter region of RGC32 gene in nonsmall cell lung cancers (NSCLCs) using a methylation-specific PCR and correlated the results with clinicopathological features.
RESULTS: RGC32 methylation was found in 45 of 173 NSCLCs (26.0%) and was related to the gene expression. RGC32 methylation was more frequent in females than in males (P<0.05). RGC32 methylation was not significantly associated with the prognosis of patients; however, when the patients were categorized by TP53 mutational status, the effect of RGC32 methylation on prognosis was significantly different between those with and without TP53 mutations (P = .005 [test for homogeneity]). Specifically, RGC32 methylation was associated with significantly worse survival in the cases with wild-type TP53, whereas it exhibited a better survival outcome in the cases with TP53 mutations.
CONCLUSIONS: The current findings suggest that methylation-associated down-regulation of RGC32 plays an important role in the pathogenesis of NSCLC, particularly in females. However, further studies with a large number of cases are needed to confirm the authors' findings.
Copyright © 2010 American Cancer Society.

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Year:  2010        PMID: 20862745     DOI: 10.1002/cncr.25451

Source DB:  PubMed          Journal:  Cancer        ISSN: 0008-543X            Impact factor:   6.860


  19 in total

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4.  Regulator of Cell Cycle Protein (RGCC/RGC-32) Protects against Pulmonary Fibrosis.

Authors:  Irina G Luzina; Violeta Rus; Virginia Lockatell; Jean-Paul Courneya; Brian S Hampton; Rita Fishelevich; Alexander V Misharin; Nevins W Todd; Tudor C Badea; Horea Rus; Sergei P Atamas
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Review 5.  Role of C5b-9 complement complex and response gene to complement-32 (RGC-32) in cancer.

Authors:  Sonia I Vlaicu; Cosmin A Tegla; Cornelia D Cudrici; Jacob Danoff; Hassan Madani; Adam Sugarman; Florin Niculescu; Petru A Mircea; Violeta Rus; Horea Rus
Journal:  Immunol Res       Date:  2013-05       Impact factor: 2.829

6.  Overexpression of response gene to complement 32 (RGC32) promotes cell invasion and induces epithelial-mesenchymal transition in lung cancer cells via the NF-κB signaling pathway.

Authors:  Qinying Sun; Xiaopeng Yao; Yunye Ning; Wei Zhang; Guowu Zhou; Yuchao Dong
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7.  Renal proteomic analysis of RGC-32 knockout mice reveals the potential mechanism of RGC-32 in regulating cell cycle.

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8.  Knockdown of response gene to complement 32 (RGC32) induces apoptosis and inhibits cell growth, migration, and invasion in human lung cancer cells.

Authors:  Ran Xu; Chao Shang; Jungang Zhao; Yun Han; Jun Liu; Kuanbing Chen; Wenjun Shi
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9.  Upregulation of the cell-cycle regulator RGC-32 in Epstein-Barr virus-immortalized cells.

Authors:  Sandra N Schlick; C David Wood; Andrea Gunnell; Helen M Webb; Sarika Khasnis; Aloys Schepers; Michelle J West
Journal:  PLoS One       Date:  2011-12-06       Impact factor: 3.240

10.  RGC-32 (Response Gene to Complement 32) Deficiency Protects Endothelial Cells From Inflammation and Attenuates Atherosclerosis.

Authors:  Xiao-Bing Cui; Jun-Na Luan; Kun Dong; Sisi Chen; Yongyi Wang; Wendy T Watford; Shi-You Chen
Journal:  Arterioscler Thromb Vasc Biol       Date:  2018-02-15       Impact factor: 8.311

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