A novel gene, <i>NMES1,</i> downregulated in human esophageal squamous cell carcinoma

Zhang, Jin; Wang, Huixin; Lu, Ailing; Hu, Gengxi; Luo, Aiping; Ding, Fang; Zhang, Jian; Wang, Xiuqin; Wu, Min; Liu, Zhihua

doi:10.1002/ijc.10600

Cited by 44 publications

(35 citation statements)

References 11 publications

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“…RRAD, encoding a protein belonging to a subfamily of Ras-related GTPbinding proteins (32), has been recently found aberrantly methylated in mesotheliomas in relationship with SV40 infection (33). Hypermethylation of NMES1 has not been previously noted in any tissue, although this gene has been reported to be expressed in normal but not in malignant esophageal tissues (34).…”

Section: Discussionsupporting

confidence: 46%

Discovery of Novel Methylation Biomarkers in Cervical Carcinoma by Global Demethylation and Microarray Analysis

Sova

Feng

Geiss

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

137

101

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A genome-wide screening study for identification of hypermethylated genes in invasive cervical cancer (ICC) was carried out to augment our previously discovered panel of three genes found to be useful for detection of ICC and its precursor neoplasia. Putatively hypermethylated and silenced genes were reactivated in four ICC cell lines by treatment with 5-aza-2V -deoxycytidine and trichostatin A and identified on expression microarrays. Thirty-nine of the 235 genes up-regulated in multiple ICC cell lines were further examined to determine the methylation status of associated CpG islands. The diagnostic use of 23 genes that were aberrantly methylated in multiple ICC cell lines were then analyzed in DNA from exfoliated cells obtained from patients with or without ICC. We show, for the first time, that aberrant methylation of six genes (SPARC, TFPI2, RRAD, SFRP1, MT1G, and NMES1) is present in a high proportion of ICC clinical samples but not in normal samples. Of these genes, SPARC and TFPI2 showed the highest frequency of aberrant methylation in ICC specimens (86.4% for either) and together were hypermethylated in all but one ICC cases examined. We conclude that expression profiling of epigenetically reactivated genes followed by methylation analysis in clinical samples is a powerful tool for comprehensive identification of methylation markers. Several novel genes identified in our study may be clinically useful for detection or stratification of ICC and/or of its precursor lesions and provide a basis for better understanding of mechanisms involved in development of ICC.

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Section: Discussionsupporting

confidence: 46%

Discovery of Novel Methylation Biomarkers in Cervical Carcinoma by Global Demethylation and Microarray Analysis

Sova

Feng

Geiss

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

137

101

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“…The functional consequences of NMES1 induction by TLR stimulation in macrophages are presently unknown. A previous study suggested that NMES1 may have a role as a tumor suppressor (22). Given that inflammation has been closely associated with carcinogenesis, elevation of NMES1 in inflammatory diseases may be a protective mechanism to prevent cellular transformation.…”

Section: Discussionsupporting

confidence: 43%

miR-147, a microRNA that is induced upon Toll-like receptor stimulation, regulates murine macrophage inflammatory responses

Liu

Friggeri

Yang

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

401

300

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Toll-like receptors (TLRs) are major receptors that enable inflammatory cells to recognize invading microbial pathogens. MicroRNAs are small non-coding RNAs that play important regulatory roles in a variety of biological processes. In this study, we found that a microRNA, miR-147, was induced upon stimulation of multiple TLRs and functioned as a negative regulator of TLR-associated signaling events in murine macrophages. We first demonstrated that the NMES1 transcript was a functional primary miR-147. miR-147 was induced in LPS-stimulated mouse macrophages and under in vivo conditions in the lungs of LPS-treated mice. Expression of miR-147 was greater after cellular activation by TLR4 than after engagement of either TLR2 or TLR3, suggesting that maximal induction of miR-147 required activation of both NF-B and IRF3. TLR4-induced miR-147 expression was both MyD88-and TRIFdependent. The miR-147 promoter was responsive to TLR4 stimulation and both NF-B and STAT1␣ bound to the miR-147 promoter. miR-147 mimics or induced expression of miR-147 decreased, whereas miR-147 knockdown increased inflammatory cytokine expression in macrophages stimulated with ligands to TLR2, TLR3, and TLR4. These data demonstrate a negative-feedback loop in which TLR stimulation induces miR-147 to prevent excessive inflammatory responses.

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“…Jiang et al (11) has reported previously that amplification of the cyclin D1 gene is observed in about 25% of primary esophageal carcinomas from the People's Republic of China. In addition, altered gene expression of some growth-or differentiationrelated genes were found recently to be associated with ESCC (12)(13)(14). Therefore, abnormalities in oncogenes and tumor suppressor genes, as well as in cell cycle regulators may contribute to esophageal carcinogenesis and malignancy development.…”

Section: Introductionmentioning

confidence: 39%

Overexpression of Aurora-A Contributes to Malignant Development of Human Esophageal Squamous Cell Carcinoma

Tong

Kong

et al. 2004

Clinical Cancer Research

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151

129

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Purpose: Aurora-A/STK15/BTAK, a centrosome-associated oncogenic protein, is implicated in the control of mitosis. Overexpression of Aurora-A has been shown to result in chromosomal aberration and genomic instability. Multiple lines of evidence indicate that Aurora-A induces cell malignant transformation. In the current study, we are interested in investigating the expression of Aurora-A in human esophageal squamous cell carcinoma (ESCC) and characterizing the association of Aurora-A with ESCCmalignant progression.Experimental Design: Aurora-A protein expression was examined in 84 ESCC tissues and 81 paired normal adjacent tissues by either immunohistochemistry or Western blot analysis. In addition, a gene-knockdown small interfering RNA technique was used in ESCC cells to investigate whether Aurora-A contributes to the ability of a tumor to grow invasively.Results: The amount of Aurora-A protein in ESCC was considerably higher than that in normal adjacent tissues. Overexpression of Aurora-A was observed in 57 of 84 (67.5%) ESCC samples. In contrast, <2% of normal adjacent tissue displayed high expression of Aurora-A. Interestingly, overexpression of Aurora-A seemed to correlate with the invasive malignancy of ESCC. Disruption of endogenous Aurora-A using small interfering RNA technique substantially suppressed cell migrating ability. Conclusion:The findings presented in this report show that Aurora-A expression is elevated in human esophageal squamous cell carcinoma and is possibly associated with tumor invasion, indicating that overexpression of Aurora-A may contribute to ESCC occurrence and progression.

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A novel gene, NMES1, downregulated in human esophageal squamous cell carcinoma

Cited by 44 publications

References 11 publications

Discovery of Novel Methylation Biomarkers in Cervical Carcinoma by Global Demethylation and Microarray Analysis

Discovery of Novel Methylation Biomarkers in Cervical Carcinoma by Global Demethylation and Microarray Analysis

miR-147, a microRNA that is induced upon Toll-like receptor stimulation, regulates murine macrophage inflammatory responses

Overexpression of Aurora-A Contributes to Malignant Development of Human Esophageal Squamous Cell Carcinoma

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