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Gene expression analysis of arecoline treated human gingival epithelial cells

ABSTRACT: To identify the presence of a novel gene in epithelial cells stimulated with arecoline, a main component of betel quid.

ORGANISM(S): Homo sapiens

PROVIDER: GSE157247 | GEO | 2020/09/02

REPOSITORIES: GEO

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Methylation array of arecoline treated human gingival epithelial cells

Project description:Identify the methylation level of genes in epithelial cells stimulated with arecoline, a main component of betel quid.

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Methylation array of arecoline treated human gingival epithelial cells

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Gene expression analysis of arecoline treated human gingival epithelial cells

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Project description:MicroRNAs (miRNAs) participate in many biological processes and have emerged as key players in carcinogenesis. In order to identify changes in miRNAs specific for betelquid-associated oral squamous cell carcinoma (OSCC), we investigated the expression profiles of 858 miRNAs in a panel of 40 pairs of OSCC specimens and their matched non-tumorous epithelial counterparts. Eighty-four miRNAs were differentially expressed in the OSCC specimens compared to the matched tissue. Among these miRNAs, 19 downregulated miRNAs located in the chromosome 14q32.2 miRNA cluster region were analyzed. This miRNA cluster resides within a parentally imprinted region known to be important in development and growth. The re-expression of miR-329 and miR-410from this cluster significantly reduced OSCC cell proliferation and invasion and downregulated Wnt-7b, an activator of the Wnt/b-catenin pathway. Furthermore, the expression of those 2 miRNAs was restored by 5-aza-2′-deoxycytidine treatment and the expression levels of the 2 miRNAs were inversely correlated with the hypermethylation of the Meg-3 promoter in OSCC cells. Specifically, arecoline, a major betel nut alkaloid, reduces miR-329 and miR-410 expression. Our results thus provide a novel molecular insight into how betel quid may contribute to oral carcinogenesis through the epigenetic silencing of tumor suppressor miRNAs targeting the Wnt/b-catenin signaling pathway. Total RNA was obtained from 40 pairs of OSCC patients with tumor specimens and their adjacent non-tumorous epithelia.

2015-01-07 | E-GEOD-45238 | biostudies-arrayexpress

OSCC CGH SriLanka vs India

Project description:In Asia, oral cancer (OC) and oral submucous fibrosis (OSF) constitute major health problems linked to use of betel quid. This work performed CGH genome-wide analysis of OC (12 from India, 12 from Sri Lanka) and OSF (6 from India) cases with normal controls.

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Gene expression profie of OSMF (Oral Submucous Fibrosis) tissues compared with the expression in normal oral tissues

Project description:ABSTRACT: Background: Oral Submucous Fibrosis (OSF) is a chronic inflammatory disease resulting in progressive fibrosis of the oral soft tissues. Habit of chewing betel quid has been proposed as an important etiological factor in the development of this disease. But the exact mechanism of pathogenesis is still not clear. Methods: We took microarray approach to identify differentially regulated genes in 10 OSF tissues against 8 pooled normal tissues using oligonucleotide arrays. Microarray results have been confirmed by qRT-PCR. Regulation of genes in epithelial and fibroblast cells was studied after treatment with arecoline, TGF-b and LAP followed by qRT-PCR. Results: Total number of genes found to be commonly regulated in OSF (p<=0.05 and Fold change>=1.5) tissues are 5288 and among them 2884 are up-regulated and 2404 are down-regulated. Extra cellular matrix genes that have been reported in OSF such as collagens, fibronectin and cytokines ET1, CTGF and TGF-b1 are among the up regulated genes. The list of up and down regulated genes also includes RARRES1, TGM2, THBS1, CHGB, MMP3, SPP1 and ALOX12, C4orf7 respectively. Analysis of microarray data revealed TGF-? pathway as a principal gene network involved in the development of OSF. Intriguingly, there was no regulation of CTGF and THBS1 in fibroblasts by arecoline. However, TGF-b1 treatment regulated all these genes in both epithelial and fibroblast cells. Conclusion: We demonstrate over expression of novel genes in OSF and suggest that OSF development involves TGF-b pathway in an epithelial-stromal cooperation. Targeting TGF-b signaling could be an alternate strategy to treat OSF. Two-condition experiment: 10 OSF tissues against 8 pooled normal tissues

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Identification of oral carcinoma miRNA involved in Wnt/b-catenin signaling

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