scholarly journals A novel tumor suppressor gene NCOA5 is correlated with progression in papillary thyroid carcinoma

2018 ◽  
Vol Volume 11 ◽  
pp. 307-311 ◽  
Author(s):  
Zhou-Ci Zheng ◽  
Qing-Xuan Wang ◽  
Wei Zhang ◽  
Xiao-Hua Zhang ◽  
Du-Ping Huang
Oncotarget ◽  
2015 ◽  
Vol 7 (5) ◽  
pp. 5830-5841 ◽  
Author(s):  
De-Tao Yin ◽  
Jianhui Xu ◽  
Mengyuan Lei ◽  
Hongqiang Li ◽  
Yongfei Wang ◽  
...  

2004 ◽  
Vol 13 (1) ◽  
pp. 41-46 ◽  
Author(s):  
Jennifer L. Hunt ◽  
Melissa Fowler ◽  
Deren Lomago ◽  
Laura Niehouse ◽  
Eizaburo Sasatomi ◽  
...  

2006 ◽  
Vol 14 (5) ◽  
pp. 1772-1779 ◽  
Author(s):  
Alfred King Yin Lam ◽  
Chung Yau Lo ◽  
Pauline Leung ◽  
Brian Hung Hin Lang ◽  
Wai Fun Chan ◽  
...  

Author(s):  
Sara Sheikholeslami ◽  
Fereidoun Azizi ◽  
Asghar Ghasemi ◽  
Abbas Alibakhshi ◽  
Hossein Parsa ◽  
...  

Background: Thyroid cancer is the fourth most common cancer in the world. Papillary thyroid carcinoma (PTC) accounts for 80% of all types of thyroid neoplasm. Epigenetic alterations such as DNA methylation are known as the main cause of different types of cancers through inactivation of tumor suppressor genes. Objectives: In the present study, the expression and methylation of suggested gene namely nucleolar protein 4 (NOL4) in PTC in comparison to multi nodular goiter (MNG) have been studied. Methods: Forty-one patients with PTC and 38 patients affected by MNG were recruited. Thyroid tissues were obtained during thyroidectomy. RNA and DNA were extracted from thyroid tissues. Quantitative RT-PCR assay was performed for determining the mRNA level of NOL4 while methylation-sensitive high resolution methylation was applied for assessing the methylation status with designing six pairs primers for six regions on gene promoter which were named from NOL4 (a) to NOL4 (f). Results: Methylation assessment of 81 CpG islands in the promoter region of NOL4 gene revealed that NOL4 (f), the nearest region to the start codon, was significantly hypermethylated in PTC cases compared to MNG cases. NOL4 level in PTC cases in comparison with MNG cases were downregulated. The methylation status and mRNA level of NOL4 (f) were associated with age of diagnosis (Age of the patient at the time of diagnosis), lymph node metastasis, and advanced stages of disease. Conclusions: These data suggested an aberrant promoter hyper-methylation of NOL4 in PTC cases may be linked with its downregulation. Therefore, NOL4 gene can be proposed as a potential tumor suppressor gene in PTC tissues.


2007 ◽  
Vol 21 (12) ◽  
pp. 3039-3049 ◽  
Author(s):  
Dong Wook Kim ◽  
Hyo Kyun Chung ◽  
Ki Cheol Park ◽  
Jung Hwan Hwang ◽  
Young Suk Jo ◽  
...  

Abstract The tumor suppressor LKB1 (STK11) is a cytoplasmic/nuclear serine/threonine kinase, defects in which cause Peutz-Jeghers syndrome (PJS) in humans and animals. Recent studies showed that loss of function of LKB1 is associated with sporadic forms of lung, pancreatic, and ovarian cancer. In cancer cells, LKB1 is inactivated by two mechanisms: mutations in its central kinase domain or complete loss of LKB1 expression. Inactivation of LKB1 is associated with progression of PJS and transformation of benign polyps into malignant tumors. This study examines the effect of LKB1 on regulation of STAT3 and expression of transcriptional targets of STAT3. The results show that LKB1 inhibits rearranged in transformation (RET)/papillary thyroid carcinoma (PTC)-dependent activation of signal transducer and activator of transcription 3 (STAT3), which is mediated by phosphorylation of STAT3 tyrosine 705 by RET/PTC. Suppression of STAT3 transactivation by LKB1 requires the kinase domain but not the kinase activity of LKB1. The centrally located kinase domain of LKB1 is an approximately 260-amino-acid region that binds to the linker domain of STAT3. Chromatin immunoprecipitation studies indicate that expression of LKB1 reduces the binding of STAT3 to its target promoters and suppresses STAT3-mediated expression of Cyclin D1, VEGF, and Bcl-xL. Knockdown of LKB1 by specific small interfering RNA led to an increase in STAT3 transactivation activity and promoted cell proliferation in the presence of RET/PTC. Thus, this study suggests that LKB1 suppresses tumor growth by inhibiting RET/PTC-dependent activation of oncogenic STAT3.


Oncogene ◽  
2011 ◽  
Vol 31 (35) ◽  
pp. 3961-3972 ◽  
Author(s):  
A Macià ◽  
P Gallel ◽  
M Vaquero ◽  
M Gou-Fabregas ◽  
M Santacana ◽  
...  

2009 ◽  
Vol 124 (2) ◽  
pp. 339-345 ◽  
Author(s):  
Wendy van Veelen ◽  
Rob Klompmaker ◽  
Martijn Gloerich ◽  
Carola J.R. van Gasteren ◽  
Eric Kalkhoven ◽  
...  

2014 ◽  
Vol 50 ◽  
pp. S31
Author(s):  
E. Minna ◽  
P. Romeo ◽  
L. De Cecco ◽  
M. Dugo ◽  
G. Cassinelli ◽  
...  

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