scholarly journals Hsa_circRNA_102002 facilitates metastasis of papillary thyroid cancer through regulating miR-488-3p/HAS2 axis

2020 ◽  
Author(s):  
Wei Zhang ◽  
Ting Liu ◽  
Tianshu Li ◽  
Xudong Zhao
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Xenograft Model ◽  
Inhibitory Effect ◽  
Circular Rnas ◽  
Papillary Thyroid ◽  
Mesenchymal Transition ◽  
Mouse Xenograft Model ◽  
And Migration

Abstract As important modulators in various physiological processes, circular RNAs (circRNAs) have been increasingly demonstrated in tumors, including papillary thyroid cancer (PTC). Hsa_circRNA_102002 (circ_102002) is a circRNA derived from alternative splicing of ubiquitin-specific peptidase 22 (USP22) transcript, the role of which needs further investigation. Our results suggested the upregulation of circ_102002 in PTC tissues and cells, and its promoting effects on epithelial–mesenchymal transition (EMT) and cell migration. Mechanism studies showed that circ_102002 could sponge microRNA-488-3p (miR-488-3p) and downregulate its expression. The target relationship between miR-488-3p and hyaluronic acid synthetase 2 (HAS2) in PTC was systematically studied. In addition, our results showed that HAS2 overexpression could restore the inhibited cell EMT and migration. Moreover, the inhibitory effect of downregulation of circ_102002 on PTC growth was evaluated in a mouse xenograft model, which involved miR-488-3p and HAS2 regulation. These findings about the signal axis of circ_102002/miR-488-3p/HAS2 may further elucidate the PTC pathogenesis and improve clinical treatment.

scholarly journals Loss of ID3 drives papillary thyroid cancer metastasis by targeting E47-mediated epithelial to mesenchymal transition

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Sunwang Xu ◽  
Caiqin Mo ◽  
Junyu Lin ◽  
Yixing Yan ◽  
Xiaoyu Liu ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Tumor Suppressor ◽  
Papillary Thyroid Cancer ◽  
Epithelial To Mesenchymal Transition ◽  
Cpg Island ◽  
Papillary Thyroid ◽  
Free Survival ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

AbstractPapillary thyroid cancer (PTC) is the main histological type of thyroid cancer and accounts for almost all increased cases worldwide. Patients with PTC exhibit a favorable prognosis, but the fact that PTC is often accompanied by a high prevalence of lymph node metastasis (LNM) means that the overall recurrence-free survival rate in PTC patients is relatively low. Herein, we identified that ID3 expression is subdued in PTC tissues and closely associated with LNM and a poor disease-free survival outcome in PTC patients. The main contributor to this gene repression is the hypermethylation of the CpG island at the promoter of ID3. Besides, we uncovered that a loss of ID3 promotes invasion and migration of PTC cells, while an ectopic overexpression of ID3 inhibits invasion and migration. Mechanistically, ID3 exhibits tumor suppressor functions in PTC cells by interacting with E47 to form heterodimers that prevent E47 binding to CDH1 promoter and maintaining CDH1 transcription and epithelial phenotype in PTC cells. Taken together, our study demonstrates that ID3 plays a tumor suppressor role in PTC and impedes metastasis by inhibiting E47-mediated epithelial to mesenchymal transition.

scholarly journals KIFC1 accelerates the proliferation, migration and invasion of papillary thyroid cancer cells via MAPK signaling

2020 ◽  
Author(s):  
Chunlei Nie ◽  
Jihua Han ◽  
Wen Bi ◽  
Lili Chen ◽  
Jiawei Yu ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Molecular Mechanisms ◽  
Epithelial Mesenchymal Transition ◽  
Mapk Signaling ◽  
Migration And Invasion ◽  
Papillary Thyroid ◽  
Differentiation Markers ◽  
Mesenchymal Transition ◽  
Extrathyroidal Invasion

Abstract Kinesin family member C1 (KIFC1) acts as a kind of minus end-directed motorized protein and is considered as an oncogene of some cancer types. However, no studies have fully elucidated its biological activity and molecular mechanisms in papillary thyroid cancer (PTC). The study focused on reporting the overexpression of KIFC1 in cell lines and tissues of PTC. Moreover, clinicopathological features analysis showed that KIFC overexpression is significantly correlated with extrathyroidal invasion and lymph node metastasis. Knockdown of KIFC1 significantly reduced cell growth, migration and invasion in PTC cells, and concomitant increased levels of differentiation markers, such as Tg and Nis. Knockdown of KIFC1 markedly increased the expression level of epithelial cell marker (E-cadherin), and decreased the expression levels of epithelial-mesenchymal transition (EMT) related transcriptional factor N-cadherin, Snail and ZEB1. Further study revealed that knockdown of KIFC1 downregulated stemness markers ALDH2 and SOX2, and inhibited the MAPK signaling cascades and downstream signaling, including p-ERK, ERK, p-JNK, JNK, MMP2, and MMP9, which can affect the expression of the EMT associated factors. Taken together, we reported that KIFC1 might promoted the proliferation, migration and invasion of PTC cells and offer a candidate molecular target for therapeutic intervention.

scholarly journals lncRNA CASC2 Enhances 131I Sensitivity in Papillary Thyroid Cancer by Sponging miR-155

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Ling Tao ◽  
Ping Tian ◽  
Li Yang ◽  
Xiangyang Guo
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Noncoding Rna ◽  
Xenograft Model ◽  
Continuous Treatment ◽  
Luciferase Assay ◽  
Papillary Thyroid ◽  
Mouse Xenograft Model ◽  
Resistant Cells

Long noncoding RNA cancer susceptibility candidate 2 (CASC2) has been reported to play an anticancer role in papillary thyroid cancer (PTC). Radioiodine (131I) is a common option for the treatment of PTC. However, the role and mechanism of CASC2 in 131I sensitivity remain unclear. In this study, 131I-resistant cells were constructed through continuous treatment of 131I. The expression levels of CASC2 and miR-155 were measured by qRT-PCR. The IC50 of 131I was analyzed by cell viability using MTT assay. Flow cytometry was conducted to determine cell apoptosis induced by 131I. The association between CASC2 and miR-155 was evaluated by luciferase assay and RNA immunoprecipitation. A mouse xenograft model was built to explore the effect of CASC2 on the growth of 131I-resistant PTC cells in vivo. Results showed that CASC2 expression was decreased in PTC tissues and cells, and low expression of CASC2 was associated with poor outcome of patients. CASC2 level was reduced in 131I-resistant cells. Knockdown of CASC2 inhibited 131I sensitivity in thyroid cancer cells. Overexpression of CASC2 enhanced 131I sensitivity in constructed resistant PTC cells. CASC2 was a decoy of miR-155, and CASC2-mediated promotion of 131I sensitivity was weakened by decreasing miR-155. Abundance of CASC2 inhibited the growth of 131I-resistant cells in vivo. As a conclusion, CASC2 increases 131I sensitivity in PTC by sponging miR-155, providing a novel target for the treatment of thyroid cancer patients with 131I resistance.

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