TFPI-2 is a putative tumor suppressor gene frequently inactivated by promoter hypermethylation in nasopharyngeal carcinoma

Wang, Shumin; Xiao, Xue; Zhou, Xiaoying; Huang, Tingting; Du, Chunping; Yu, Nana; Mo, Yuchang; Lin, Longde; Zhang, Jinyan; Ma, Ning; Murata, Mariko; Zhang, Zhe

doi:10.1186/1471-2407-10-617

Cited by 52 publications

(34 citation statements)

References 29 publications

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“…frequently methylated in various other cancers as well as in lung cancer (Glöckner et al, 2009;Takadaa et al, 2010;Wang et al, 2010). Silencing of the TFPI-2 gene by hypermethylation might contribute to tumor progression in NSCLC (Rollin et al, 2005).…”

Section: Deoxycytidine Effects On Proliferation Of Nsclc A549 Cells Amentioning

confidence: 99%

Effect of 5-aza-2'-deoxycytidine on Cell Proliferation of Non-small Cell Lung Cancer Cell Line A549 Cells and Expression of the TFPI-2 Gene

Dong

Liang²,

Zhu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Section: Deoxycytidine Effects On Proliferation Of Nsclc A549 Cells Amentioning

confidence: 99%

Effect of 5-aza-2'-deoxycytidine on Cell Proliferation of Non-small Cell Lung Cancer Cell Line A549 Cells and Expression of the TFPI-2 Gene

Dong

Liang²,

Zhu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…Increased SER-PINE1 expression reduced migration by normal prostate cells [89]. Consistent with HGF suppression of TFPI, decreased TFPI expression has been correlated with increased cell motility, invasion and tumor metastasis in breast and pancreatic cancers, glioblastoma, melanoma and nasopharyngeal carcinoma [90][91][92][93][94]. Tissue factor pathway inhibitor (TFPI) also interferes with endothelial cell migration by inhibiting the Erk pathway and focal adhesion proteins [95].…”

Section: Metabolism and Ion Transport (Asns And Scnn1g)mentioning

confidence: 83%

Expression array analysis of the hepatocyte growth factor invasive program

Cecchi

Lih

Lee

et al. 2015

Clin Exp Metastasis

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Signaling by human hepatocyte growth factor (hHGF) via its cell surface receptor (MET) drives mitogenesis, motogenesis and morphogenesis in a wide spectrum of target cell types and embryologic, developmental and homeostatic contexts. Oncogenic pathway activation also contributes to tumorigenesis and cancer progression, including tumor angiogenesis and metastasis, in several prevalent malignancies. The HGF gene encodes full-length hHGF and two truncated isoforms known as NK1 and NK2. NK1 induces all three HGF activities at modestly reduced potency, whereas NK2 stimulates only motogenesis and enhances HGF-driven tumor metastasis in transgenic mice. Prior studies have shown that mouse HGF (mHGF) also binds with high affinity to human MET. Here we show that, like NK2, mHGF stimulates cell motility, invasion and spontaneous metastasis of PC3M human prostate adenocarcinoma cells in mice through human MET. To identify target genes and signaling pathways associated with motogenic and metastatic HGF signaling, i.e., the HGF invasive program, gene expression profiling was performed using PC3M cells treated with hHGF, NK2 or mHGF. Results obtained using Ingenuity Pathway Analysis software showed significant overlap with networks and pathways involved in cell movement and metastasis. Interrogating The Cancer Genome Atlas project also identified a subset of 23 gene expression changes in PC3M with a strong tendency for co-occurrence in prostate cancer patients that were associated with significantly decreased disease-free survival.

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“…TFPI-2 is a candidate TSG with important roles in carcinogenesis and metastasis in human cancers. Transcriptional silencing by promoter hypermethylation of TFPI-2 has been observed in some human cancers including NPC Wang et al 2010). Using methylation-specific PCR and bisulfate genomic sequencing, Wang et al (2010) found that TFPI-2 was aberrantly methylated in 88.6 % (62/70) of NPC primary tumors, but not in normal nasopharyngeal epithelia.…”

Section: Tissue Inhibitor Of Metalloproteinase-3 (Timp-3) Genementioning

confidence: 98%

“…Transcriptional silencing by promoter hypermethylation of TFPI-2 has been observed in some human cancers including NPC Wang et al 2010). Using methylation-specific PCR and bisulfate genomic sequencing, Wang et al (2010) found that TFPI-2 was aberrantly methylated in 88.6 % (62/70) of NPC primary tumors, but not in normal nasopharyngeal epithelia. The authors suggested that epigenetic inactivation of TFPI-2 by promoter hypermethylation is common and can be a specific marker for the diagnosis of NPC.…”

Section: Tissue Inhibitor Of Metalloproteinase-3 (Timp-3) Genementioning

confidence: 98%

DNA Methylation as a Biomarker in Nasopharyngeal Carcinoma

Ksiâa¹,

Trimèche²

2014

Biomarkers in Cancer

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Nasopharyngeal carcinoma (NPC) is a malignancy with remarkable ethnic and geographic distribution. Initially, point mutations and chromosomal deletions were considered to be the major events involved in the inactivation of tumor-suppressor genes in NPC. The discovery that many tumor-suppressor genes can also be inactivated by hypermethylation of the CpG islands in their promoter region clearly indicates that epigenetic events also play an important role as alternative mechanisms in NPC carcinogenesis.In this chapter, we update current information on methylated genes associated with the development and progression of NPC. Promoter hypermethylation of critical genes could be potential biomarkers and therapeutic targets for NPC.Several genes have been investigated for methylation in the promoter region in NPC. These methylated genes are involved in critical pathways, such as DNA repair, cell cycle regulation, and invasion/ metastasis.The role of hypermethylated genes in the deregulation of critical pathways in NPC is now well known. Besides their role on the pathogenesis of NPC, results from many investigations have provided additional information on the potential role of hypermethylated genes as predictive biomarkers in the development and progression of NPC.

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TFPI-2 is a putative tumor suppressor gene frequently inactivated by promoter hypermethylation in nasopharyngeal carcinoma

Cited by 52 publications

References 29 publications

Effect of 5-aza-2'-deoxycytidine on Cell Proliferation of Non-small Cell Lung Cancer Cell Line A549 Cells and Expression of the TFPI-2 Gene

Effect of 5-aza-2'-deoxycytidine on Cell Proliferation of Non-small Cell Lung Cancer Cell Line A549 Cells and Expression of the TFPI-2 Gene

Expression array analysis of the hepatocyte growth factor invasive program

DNA Methylation as a Biomarker in Nasopharyngeal Carcinoma

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