Association of Cigarette Smoking with Aberrant Methylation of the Tumor Suppressor Gene RAR?2 in Papillary Thyroid Cancer

2019 ◽

Vol 9 (5) ◽

pp. 694-699

Author(s):

Xiaojie Gao ◽

Zhenyu Hou ◽

Shucheng Wang

Keyword(s):

Thyroid Cancer ◽

Tumor Suppressor ◽

Tumor Suppressor Gene ◽

Papillary Thyroid Cancer ◽

Methylation Level ◽

Mrna Level ◽

Suppressor Gene ◽

Papillary Thyroid ◽

Increased Risk ◽

P73 Gene

This study aimed to investigate the association between methylation in the promoter region of the p73 gene and the clinical features papillary thyroid cancer. Forty-two pairs of papillary thyroid cancer and corresponding paracancerous tissues and blood samples from January to June 2015 were enrolled in this study. The methylation level of the p73 gene and p73 mRNA level were detected by methylation-specific PCR and quantitative reverse transcription-PCR. The correlation between the methylation level of p73 gene and p73 mRNA level was analyzed. The methylation status of p73 and p16 in plasma were also detected, and the correlation between them was analyzed. The results showed that p73 methylation was found at CG sites in 28 cancer tissues, which mainly located at positions 21, 22, 23 CG sites, but methylation was not identified at CG sites in paracancerous tissues (P < 0.01). The methylation level of the p73 gene was negatively correlated with p73 mRNA level (P < 0.01). Methylation of p73 gene was correlated with lymph node metastasis, but not age, sex, clinical stage of the patients. Methylation of p73 in plasma was correlated with methylation of tumor suppressor gene p16, which increased the risk of papillary thyroid cancer. In conclusion, we found that hypermethylation of the p73 gene is associated with the development and metastasis of papillary thyroid cancer, which may be suggested as a new candidate tumor suppressor gene in papillary thyroid cancer.

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Serum deprivation response functions as a tumor suppressor gene in papillary thyroid cancer

Clinical Genetics ◽

10.1111/cge.13609 ◽

2019 ◽

Vol 96 (5) ◽

pp. 418-428 ◽

Cited By ~ 2

Author(s):

Qing‐Xuan Wang ◽

En‐Dong Chen ◽

Ye‐Feng Cai ◽

Yi‐Li Zhou ◽

Si‐Yang Dong ◽

...

Keyword(s):

Thyroid Cancer ◽

Tumor Suppressor ◽

Tumor Suppressor Gene ◽

Papillary Thyroid Cancer ◽

Suppressor Gene ◽

Serum Deprivation ◽

Response Functions ◽

Papillary Thyroid

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Association of aberrant methylation of tumor suppressor genes with tumor aggressiveness and BRAF mutation in papillary thyroid cancer

International Journal of Cancer ◽

10.1002/ijc.22110 ◽

2006 ◽

Vol 119 (10) ◽

pp. 2322-2329 ◽

Cited By ~ 117

Author(s):

Shuiying Hu ◽

Dingxie Liu ◽

Ralph P. Tufano ◽

Kathryn A. Carson ◽

Eli Rosenbaum ◽

...

Keyword(s):

Thyroid Cancer ◽

Tumor Suppressor ◽

Papillary Thyroid Cancer ◽

Braf Mutation ◽

Tumor Suppressor Genes ◽

Aberrant Methylation ◽

Papillary Thyroid ◽

Tumor Aggressiveness ◽

Suppressor Genes

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ABERRANT METHYLATION OF P16 TUMOR SUPPRESSOR GENE AND RETINOIC ACID RECEPTOR B2 IN MALIGNANT PLEURAL EFFUSION

CHEST Journal ◽

10.1378/chest.132.4_meetingabstracts.591a ◽

2007 ◽

Vol 132 (4) ◽

pp. 591A

Author(s):

Junghun Huh ◽

Choonhee Son Son ◽

Dookyung Yang ◽

Sookeol Lee ◽

Ki-Nam Kim ◽

...

Keyword(s):

Retinoic Acid ◽

Pleural Effusion ◽

Tumor Suppressor ◽

Tumor Suppressor Gene ◽

Malignant Pleural Effusion ◽

Retinoic Acid Receptor ◽

Suppressor Gene ◽

Aberrant Methylation ◽

Acid Receptor

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Mitogen-Inducible Gene-6 Is a Multifunctional Adaptor Protein with Tumor Suppressor-Like Activity in Papillary Thyroid Cancer

Molecular Endocrinology ◽

10.1210/mend.25.2.zmg373a ◽

2011 ◽

Vol 25 (2) ◽

pp. 373-373

Author(s):

Chi-Iou Lin ◽

Jinyan Du ◽

Wen Shen ◽

Edward E. Whang ◽

David B. Donner ◽

...

Keyword(s):

Thyroid Cancer ◽

Tumor Suppressor ◽

Papillary Thyroid Cancer ◽

Adaptor Protein ◽

Papillary Thyroid ◽

Inducible Gene

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Mitogen-Inducible Gene-6 Is a Multifunctional Adaptor Protein with Tumor Suppressor-Like Activity in Papillary Thyroid Cancer

Endocrine Reviews ◽

10.1210/edrv.32.1.zef157b ◽

2011 ◽

Vol 32 (1) ◽

pp. 157-158

Author(s):

Chi-Iou Lin ◽

Jinyan Du ◽

Wen Shen ◽

Edward E. Whang ◽

David B. Donner ◽

...

Keyword(s):

Thyroid Cancer ◽

Tumor Suppressor ◽

Papillary Thyroid Cancer ◽

Adaptor Protein ◽

Papillary Thyroid ◽

Inducible Gene

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NTRK3 as a novel tumor suppressor gene in colorectal cancer.

Journal of Clinical Oncology ◽

10.1200/jco.2012.30.4_suppl.469 ◽

2012 ◽

Vol 30 (4_suppl) ◽

pp. 469-469

Author(s):

Yanxin Luo ◽

Andrew Kaz ◽

Samornmas Kanngurn ◽

William M. Grady

Keyword(s):

Colorectal Cancer ◽

Colon Cancer ◽

Tumor Suppressor ◽

Cancer Cells ◽

Tumor Suppressor Gene ◽

Suppressor Gene ◽

Aberrant Methylation ◽

Colon Cancer Cells ◽

Colon Adenomas ◽

Colon Cancer Cell Lines

469 Background: Neurotrophin tyrosine kinase receptor 3 (NTRK3) is a receptor tyrosine kinase that has been shown to be an oncogene in breast cancer and possibly in hepatocellular carcinoma. NTRK3 is a trophic dependence receptor, which is a recently described class of receptors that initiate signaling in both the ligand bound and unbound states. Through a genome-wide screen for aberrantly methylated genes, we identified aberrantly methylated NTRK3 as a frequently methylated gene in colon cancer. The aim for the present study is to determine if NTRK3 is an epigenetically silenced tumor suppressor gene in colorectal cancer. Methods: NTRK3 promoter methylation was analyzed in human colon cancer cell lines, normal colon epithelium tissue, colorectal adenomas and colorectal cancers using quantitative methylation-specific PCR and bisulfite sequencing. NTRK3 mRNA and protein expression were studied using quantitative real-time PCR, immunohistochemistry and western blotting respectively. The tumor suppressor function of NTRK3 was examined by assessing the effect of NTRK3 on cell apoptosis, cell migration and in vitro colony formation assays in colon cancer cell lines stably transfected with an NTRK3 expression construct in the presence or absence of NT-3. Results: NTRK3 is methylated in 60% of colon adenomas and in 57% of colorectal cancers. The aberrant methylation of NTRK3 suppresses NTRK3 expression and releases colon cancer cells from NTRK3 mediated apoptosis induced by the expression of NTRK3 in the absence of the ligand NT-3 via the activation of MAPK/ERK pathway. Methylation of NTRK3 also releases colon cancer cells from NTRK3 mediated suppression of motility and anchorage independent growth. The addition of NT3 to colon cancer cells transfected with NTRK3 inhibits the tumor suppressor effects of NTRK3. Conclusions: The aberrant methylation of NTRK3 is likely functionally relevant for colorectal cancer formation as NTRK3 appears to be a conditional tumor suppressor gene in the colon depending on the expression status of its ligand NT-3. NTRK3 is a novel aberrantly methylated conditional tumor suppressor gene that is frequently methylated in colon adenomas and cancers and whose discovery reveals possible novel treatment approaches to colon cancer.

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