scholarly journals miR‐451a inhibits cancer growth, epithelial‐mesenchymal transition and induces apoptosis in papillary thyroid cancer by targeting PSMB8

2019 ◽  
Vol 23 (12) ◽  
pp. 8067-8075 ◽  
Author(s):  
Xinlong Fan ◽  
Yuejiao Zhao
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Growth ◽  
Papillary Thyroid ◽  
Mesenchymal Transition

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 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.

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