scholarly journals Association of Pre-miR-146a rs2910164 Polymorphism with Papillary Thyroid Cancer

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Xin Zhang ◽  
Yulu Gu ◽  
Xiaoli Liu ◽  
Yaqin Yu ◽  
Jieping Shi ◽  
...  

The incidence rate of papillary thyroid cancer (PTC) has increased over the past decades, but the pathogenesis remains unclear. rs2910164, located in pre-miR-146a, has been studied in PTCs with different ethnicity, but the results were inconsistent. Here we evaluate the association between rs2910164 polymorphism and PTC and investigate the effect of this polymorphism on patients’ clinicopathological characteristics. 1238 PTC patients and 1275 controls, all Han population, from Northern China, were included in our study. rs2910164 was genotyped using Matrix-Assisted Laser Desorption/Ionization Time of Flight Mass Spectrometry (MALDI-TOF-MS). Analysis of inheritance model was performed using the SNPStats program. Strength of association was assessed by odds ratio (OR) and 95% confidence interval (CI). Overall, no statistical difference in rs2910164 genotype distribution and allelic frequencies between cases and controls was found, and patients with different genotypes had similar clinicopathological characteristics in terms of stage, location, concurrent of benign thyroid tumor, and thyroiditis, while, as the number of G alleles increased, proportion of patients aged ≥45 years and those without metastasis increased (Ptrend<0.001andPtrend=0.003, resp.). However, no association remained significant after Bonferroni correction under any model of inheritance. Our results suggest no association between rs2910164 polymorphism with PTC and patients’ clinicopathological characteristics.

2021 ◽  
Author(s):  
Han-ning Li ◽  
Hui-min Zhang ◽  
Xing-rui Li ◽  
Jun Wang ◽  
Tao Xu ◽  
...  

Abstract Background Papillary thyroid cancer (PTC) is the most common endocrine malignancy, despite marked achieves in recent decades, the mechanisms underlying the pathogenesis and progression for PTC are incomplete. Accumulating evidence shows that γ-glutamylcyclotransferase (GGCT), an enzyme participated in glutathione homeostasis that is elevated in multiple types of tumors, represents an attractive therapeutic target. Methods Bioinformatics, immunohistochemistry (IHC), qRT-PCR and western blot (WB) assays were used to determine the elevation of GGCT in PTC. The biological functions of GGCT were examined using CCK8, wound healing and transwell assays. Subcutaneous xenograft and tail vein pulmonary metastatic mouse models were constructed to determine the effect of GGCT on tumorigenicity and metastasis in vivo. The effect of miR-205-5p on GGCT and the relationship between these two molecules were examined by dual luciferase reporter assay, RNA-RNA pull down assay as well as the rescue experiments both in vitro and in vivo. The interaction between GGCT and CD44 was assessed by co-immunoprecipitation (Co-IP) and IHC assays. Results Our results showed that GGCT expression is upregulated in PTC, correlates with more aggressive clinicopathological characteristics and worse prognosis. GGCT knockdown inhibited the cell proliferation, migratory and invasion ability of PTC cells and reduced the expression of mesenchymal markers (N-cadherin, CD44, MMP-2 and MMP9) while increased epithelial marker (E-cadherin) in PTC cells. We confirmed binding of miR-205-5p on the 3’-UTR regions of GGCT and delivery of miR-205-5p reversed the pro-malignant capacity of GGCT both in vitro and in vivo. Lastly, we found GGCT interacted with and stabilized CD44 in PTC cells. Conclusions Our findings illustrate a novel signaling pathway, miR-205-5p/GGCT/CD44, that involves in the carcinogenesis and progression of PTC. Development of miR-205-mimics or GGCT inhibitors as potential therapeutics for PTC may have remarkable applications.


2015 ◽  
Vol 100 (4) ◽  
pp. 1619-1629 ◽  
Author(s):  
Young Ah Lee ◽  
Hae Woon Jung ◽  
Hwa Young Kim ◽  
Hoonsung Choi ◽  
Hyun-Young Kim ◽  
...  

Context:Large-sample studies with long-term follow-up data are limited for pediatric patients with thyroid cancer.Objective:Secular changes in clinicopathological characteristics and outcomes in pediatric patients with thyroid cancer were investigated and compared with those of adults.Design and Patients:A retrospective review of 150 pediatric patients with thyroid cancer managed between 1980 and 2013 was conducted. The long-term outcomes of 124 patients followed up for 12 months or longer were evaluated. Predictors of recurrence-free survival (RFS) in pediatric patients with papillary thyroid cancer (ped-PTC group) were compared with those of 3071 adult patients.Results:The proportion of small tumors (&lt;1 cm) increased from 9.0% before 2010 to 36.8% after 2010 (P &lt; .001); however, neither pathological presentations such as multifocality, extrathyroidal extension (ETE), lymph node (LN) metastasis, or lung metastasis nor the RFS rate changed over time. The 5- and 10-year recurrence rates were 14.5% and 34.4% in pediatric patients, respectively. In respective analyses of the ped-PTC group and patients of all ages with papillary thyroid cancer (all ages group), the rates of ETE, LN metastasis, and lung metastasis were higher with younger age (all P for trend &lt;.05). RFS was lower in the pediatric than the adult patients aged 20–54 years (P &lt; .005) and was comparable with that of older patients (≥55 y). Only tumor multifocality and size predicted recurrence in the ped-PTC group (P &lt; .05), whereas LN metastasis and ETE also predicted recurrence in the all-ages group (P &lt; .01). Among patients in the all-ages group with multifocal tumors, pediatric patients had the lowest RFS (P &lt; .05).Conclusions:The pathological characteristics and recurrence rates of pediatric thyroid cancer have not changed over 33 years. Although younger patients present with more advanced disease, multifocality rather than age at diagnosis predicted recurrence. Recurrence was higher in pediatric than adult patients with multifocal papillary thyroid cancer.


2020 ◽  
Vol 72 (1) ◽  
pp. 31-36
Author(s):  
Lidija Todorovic ◽  
Vesna Mandusic ◽  
Biljana Vucetic-Tadic ◽  
Vladan Zivaljevic ◽  
Ivan Paunovic ◽  
...  

A growing number of studies suggest a tumor suppressive role and potential prognostic significance of miR- 30a-3p in different types of cancer. However, relatively few studies have focused on this microRNA in neoplastic thyroid lesions, including papillary thyroid cancer (PTC). The aim of our study was to shed more light on the potential involvement and clinical relevance of miR-30a-3p in this type of cancer. We examined the expression levels of this microRNA in 42 pairs of PTCs and matched non-tumor thyroid tissues using quantitative RT-PCR. We analyzed their association with clinical and histopathological parameters. The results revealed that miR-30a-3p was significantly downregulated in the majority of PTC tissues compared to corresponding non-tumor tissues. Moreover, decreased expression of miR-30a-3p was associated with advanced clinical stage, presence of multiple tumor foci and capsular invasion, suggesting a role in aggressive disease. Although the role of this microRNA and its prognostic utility remain to be elucidated, the presented data suggest that downregulated expression of miR-30a-3p indicates poorer prognosis in PTC patients, warranting further investigations.


Author(s):  
Ying Ye ◽  
Yanan Song ◽  
Juhua Zhuang ◽  
Saifei He ◽  
Jing Ni ◽  
...  

Long noncoding RNA CCAL has been reported to promote tumor progression in various human cancers, including hepatocellular carcinoma, osteosarcoma, and colorectal cancer. However, the role of CCAL in papillary thyroid cancer remains largely unknown. In the present study, we found that the expression of CCAL was upregulated in papillary thyroid tumor tissues compared to adjacent normal tissues. Moreover, the expression of CCAL was positively related with papillary thyroid cancer severity and TNM stage and predicated poor prognosis. Besides, we found that knockdown of CCAL significantly inhibited papillary thyroid cancer cell proliferation, migration, and invasion in vitro and reduced tumor growth and metastasis in vivo. We found that knockdown of CCAL dramatically decreased the expression of NOTCH1 and suppressed the activation of the NOTCH1 signaling pathway. Furthermore, overexpression of NOTCH1 rescued the proliferation, migration, and invasion in papillary thyroid cancer cells. Taken together, our data indicated that CCAL promoted papillary thyroid cancer development and progression by activation of the NOTCH1 pathway, which provided a new insight on the design of therapeutic targets.


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