scholarly journals LncRNA CRNDE promotes cell proliferation, invasion and migration by competitively binding miR-384 in papillary thyroid cancer

Oncotarget ◽  
2017 ◽  
Vol 8 (66) ◽  
pp. 110552-110565 ◽  
Author(s):  
Honggang Sun ◽  
Liqin He ◽  
Lan Ma ◽  
Tao Lu ◽  
Jianguo Wei ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Papillary Thyroid ◽  
Invasion And Migration ◽  
And Migration

scholarly journals A 5′-tRNA halve, tiRNA-Gly promotes cell proliferation and migration via binding to RBM17 and inducing alternative splicing in papillary thyroid cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Litao Han ◽  
Hejing Lai ◽  
Yichen Yang ◽  
Jiaqian Hu ◽  
Zhe Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Alternative Splicing ◽  
Papillary Thyroid Cancer ◽  
Rna Binding ◽  
Rna Binding Protein ◽  
Papillary Thyroid ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background tRNA-derived small noncoding RNAs (sncRNAs) are mainly categorized into tRNA halves (tiRNAs) and fragments (tRFs). Biological functions of tiRNAs in human solid tumor are attracting more and more attention, but researches concerning the mechanisms in tiRNAs-mediated tumorigenesis are rarely. The direct regulatory relationship between tiRNAs and splicing-related proteins remain elusive. Methods Papillary thyroid carcinoma (PTC) associated tRNA fragments were screened by tRNA fragments deep sequencing and validated by qRT-PCR and Northern Blot in PTC tissues. The biological function of tRNA fragments were assessed by cell counting kit, transwells and subcutaneous transplantation tumor of nude mice. For mechanistic study, tRNA fragments pull-down, RNA immunoprecipitation, Western Blot, Immunofluorescence, Immunohistochemical staining were performed. Results Herein, we have identified a 33 nt tiRNA-Gly significantly increases in papillary thyroid cancer (PTC) based on tRFs & tiRNAs sequencing. The ectopic expression of tiRNA-Gly promotes cell proliferation and migration, whereas down-regulation of tiRNA-Gly exhibits reverse effects. Mechanistic investigations reveal tiRNA-Gly directly bind the UHM domain of a splicing-related RNA-binding protein RBM17. The interaction with tiRNA-Gly could translocate RBM17 from cytoplasm into nucleus. In addition, tiRNA-Gly increases RBM17 protein expression via inhibiting its degradation in a ubiquitin/proteasome-dependent way. Moreover, RBM17 level in tiRNA-Gly high-expressing human PTC tissues is upregulated. In vivo mouse model shows that suppression of tiRNA-Gly decreases RBM17 expression. Importantly, tiRNA-Gly can induce exon 16 splicing of MAP4K4 mRNA leading to phosphorylation of downstream signaling pathway, which is RBM17 dependent. Conclusions Our study firstly illustrates tiRNA-Gly can directly bind to RBM17 and display oncogenic effect via RBM17-mediated alternative splicing. This fully novel model broadens our understanding of molecular mechanism in which tRNA fragment in tumor cells directly bind RNA binding protein and play a role in alternative splicing.

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 Long noncoding RNA CASC7 inhibits the proliferation and migration of papillary thyroid cancer cells by inhibiting miR-34a-5p

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Wencong Sun ◽  
Detao Yin
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Cancer Susceptibility ◽  
Luciferase Reporter ◽  
Papillary Thyroid ◽  
And Migration ◽  
Proliferation And Migration

AbstractLong noncoding RNAs (lncRNAs) play an essential role in the progression of papillary thyroid cancer (PTC). However, the expression and function of lncRNA cancer susceptibility candidate 7 (CASC7) in PTC remain unknown. The purpose of this study was to investigate the role and molecular mechanism of CASC7 in regulating PTC cell behavior. The expression of CASC7, miR-34a-5p, and tumor protein P73 (TP73) was determined by qRT-PCR and western blot. Cell proliferation was examined by MTT assay. Cell apoptosis was assessed by flow cytometry following Annexin V and PI staining. Cell migration was determined by Transwell migration assay. The interaction between miR-34a-5p and CASC7 or TP73 was examined by luciferase reporter assay. CASC7 and TP73 expression were significantly lower, whereas miR-34a-5p expression was higher in PTC tissues than the adjacent normal tissues. Furthermore, CASC7 overexpression inhibited cell proliferation and migration, whereas facilitated cell apoptosis in human PTC cell lines (K1 and TPC-1). Mechanistically, CASC7 acted as a sponge of miR-34a-5p to upregulate TP73 expression. Moreover, miR-34a-5p mimic transfection could abate the CASC7-regulated PTC cell proliferation, migration, and apoptosis. Collectively, CASC7 inhibited the proliferation and migration of PTC cells by sponging miR-34a-5p to upregulate TP73 expression.

scholarly journals Long Noncoding RNA LOC100129940-N Is Upregulated in Papillary Thyroid Cancer and Promotes the Invasion and Progression

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Manting Choy ◽  
Yan Guo ◽  
Hai Li ◽  
Guohong Wei ◽  
Runyi Ye ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Noncoding Rnas ◽  
Papillary Thyroid ◽  
Invasion And Migration ◽  
Downstream Target ◽  
And Migration

Thyroid cancer is the most common endocrine malignancy, and its incidence has increased rapidly in recent decades worldwide. Papillary thyroid cancer (PTC) is the most common type of all thyroid cancers. The molecular mechanisms underlying the disease still need to be further investigated. Long noncoding RNAs (lncRNAs), a class of noncoding RNAs (ncRNAs) longer than 200 nucleotides, are aberrantly expressed in malignant diseases, including PTC. Here, we identified a novel isoform of LOC100129940 and designated it as LOC100129940-N. We demonstrated that the expression level of LOC100129940-N was elevated in PTC, indicating that LOC100129940-N may be involved in PTC development and progression. Moreover, our results showed that overexpression of LOC100129940-N promoted, whereas silencing of LOC100129940-N suppressed, PTC cell proliferation, invasion, and migration. Mechanistically, LOC100129940-N played an important role in activating Wnt/β-catenin signaling and upregulating downstream target genes. Taken together, we demonstrate that LOC100129940-N promotes the activation of Wnt/β-catenin signaling, which in turn regulates the downstream target genes, thereby enhancing invasion and progression of PTC.

scholarly journals ciRS-7 Promotes the Proliferation and Migration of Papillary Thyroid Cancer by Negatively Regulating the miR-7/Epidermal Growth Factor Receptor Axis

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Jun-ya Han ◽  
Si Guo ◽  
Na Wei ◽  
Rui Xue ◽  
Wencai Li ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Thyroid Cancer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Papillary Thyroid Cancer ◽  
Growth Factor Receptor ◽  
Papillary Thyroid ◽  
Invasion And Migration ◽  
Epidermal Growth ◽  
And Migration

Purpose. The incidence of papillary thyroid cancer (PTC) is increasing, and traditional diagnostic methods are unsatisfactory. Therefore, identifying novel prognostic markers is very important. ciRS-7 has been found to play an important role in many cancers, but its role in PTC has not been reported. This study was performed to evaluate the biological role and mechanism of ciRS-7 in PTC. Material and Methods. The expression of ciRS-7 in PTC tissues and the matched adjacent tissues was determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The PTC cell lines (TPC-1 and BCPAP) were used to evaluate the role of ciRS-7. ciRS-7-siRNA and overexpression plasmid were constructed and transfected into PTC cells. A CCK-8 assay and colony formation assay were performed to explore the effects of ciRS-7 on cell proliferation. Annexin V/PI staining and FACS detection were used to detect cell apoptosis. Wound healing assay was performed to detect cell migration. A transwell assay was conducted to explore the effects of ciRS-7 on invasion and migration. Western blotting was performed to evaluate protein expression. The luciferase reporter system was used to determine the underlying mechanism of miR-7. Result. ciRS-7 was highly expressed in PTC tissues and cell lines compared with the corresponding controls. In vitro study showed that ciRS-7 silencing suppressed proliferation, migration, and invasion of TPC-1 and BCPAP. Mechanistically, the effects of ciRS-7 on invasion and migration may be related to epithelial-mesenchymal transition (EMT). ciRS-7 silencing could attenuate effects on PTC cells induced by miR-7 knockdown. Epidermal growth factor receptor (EGFR), which was demonstrated to be a target of miR-7, decreased significantly in ciRS-7-siRNA PTC cells. Overexpression of EGFR also attenuated effects of PTC cells induced by silencing ciRS-7. Conclusion. ciRS-7 was significantly upregulated in PTC tissues, and it promoted the progression of PTC by regulating the miR-7/EGFR axis. ciRS-7 is a promising prognostic biomarker and therapeutic target in PTC.

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