LncRNA n384546 promotes thyroid papillary cancer proliferation and migration by targeting miR-145-5p to regulate AKT3
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE124841 | GEO | 2019/06/16
REPOSITORIES: GEO
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Project description:lncRNA n384546 promotes thyroid papillary cancer proliferation and migration by targeting miR-145-5p to regulate AKT3
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2015-02-24 | E-GEOD-66177 | biostudies-arrayexpress
Project description:Akt is a robust oncogene that plays key roles in the development and progression of many cancers, including glioma. We evaluated the differential propensities of the Akt isoforms toward progression in the well-characterized RCAs/Ntv-a mouse model of PDGFB-driven low grade glioma. A constitutively active myristoylated form of Akt1 did not induce high-grade glioma (HGG). In stark contrast, Akt2 and Akt3 showed strong progression potential with 78% and 97% of tumors diagnosed as HGG, respectively. We further revealed that significant variations in polarity and hydropathy values among the Akt isoforms in both the pleckstrin homology domain (P domain) and regulatory domain (R domain) were critical in mediating glioma progression. Gene expression profiles from representative Akt-derived tumors indicated dominant and distinct roles for Akt3, consisting primarily of DNA repair pathways. TCGA data from human GBM closely reflected the DNA repair function, as Akt3 was significantly correlated with a 76 gene signature DNA repair panel. Consistently, compared to Akt1 and Akt2 overexpression models, Akt3-expressing human GBM cells had enhanced activation of DNA repair proteins, leading to increased DNA repair and subsequent resistance to radiation and temozolomide. Given the wide range of Akt3-amplified cancers, Akt3 may represent a key resistance factor.
2015-02-24 | GSE66177 | GEO
Project description:Long noncoding RNAs (lncRNAs) have been proved to play important roles in cancer biology. To understand their expression profile and potential functions in papillary thyroid carcinoma (PTC), we investigated the lncRNA and mRNA expression in PTC and paired adjacent noncancerous thyroid tissues using microarray analysis.
2015-07-16 | GSE66783 | GEO
Project description:Mice with thyroid-specific expression of oncogenic BRAF (Tg-Braf) develop papillary thyroid cancers (PTC) that are locally invasive and have well-defined foci of poorly differentiated thyroid carcinoma (PDTC). To investigate the PTC-PDTC progression, we performed a microarray analysis using RNA from paired samples of PDTC and PTC collected from the same animals by laser capture microdissection. Analysis of 8 paired samples revealed a profound deregulation of genes involved in cell adhesion and intracellular junctions, with changes consistent with an epithelial-mesenchymal transition (EMT). This was confirmed by IHC, as vimentin expression was increased and E-cadherin lost in PDTC compared to adjacent PTC. Moreover, PDTC stained positively for phospho-Smad2, suggesting a role for transforming growth factor-beta (TGFbeta) in mediating this process. Accordingly, TGFbeta induced EMT in primary cultures of thyroid cells from Tg-Braf mice, whereas wild-type thyroid cells retained their epithelial features. TGFbeta-induced Smad2 phosphorylation, transcriptional activity and induction of EMT required MAPK pathway activation in Tg-Braf thyrocytes. Hence, tumor initiation by oncogenic BRAF renders thyroid cells susceptible to TGFbeta-induced EMT, through a MAPK-dependent process. Comparing the transcription profiles of 8 pairs of murine poorly differentiated thyroid cancer and papillary thyroid cancer collected from the same animals by laser capture microdissection. Co-hybridizations were done in triplicate with a single dye flip.
2011-03-22 | E-GEOD-27668 | biostudies-arrayexpress
Project description:Papillary thyroid cancer (PTC) is a common endocrine tumor with rapidly increasing incidence in recent years. Although the majority of PTC are relatively indolen and have a good prognosis, it still has a certain proportion of PTC which is highly aggressive with lymphatic metastasis, iodine resistance and easy to recur. Circular RNAs as an class of noncoding RNAs are linked to a variety of tumor processes including PTC. In the current study, a circRNA deep sequencing was performed to identify alterations in circRNA expression levels of PTC tissues. CircTIAM1 was then selected as its increased expression in PTC and associated with migration, apoptosis and proliferation of PTC in vivo and in vitro. Mechanistically, circTIAM1 acted as a sponge of miR-646 and functioned in PTC through targeting mir-646 and HNRNPA1. Fluorescence in situ hybridization (FISH) and luciferase reporter assays further confirmed these connerctions. Overall, our results reveal an important oncogenic role of circTIAM1 in PTC and provide a potentially effective therapeutic strategy for PTC progression.
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Project description:miR-145 is downregulated in multiple cancers. The introduction of miR-145 could alleviate the tumor burden in the pancreatic cancer mouse model. However, how miR-145 mediates the tumor suppression is still an open question. In this study, we aimed to identify the targets of miR-145 using a SILAC approach.
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Project description:Mice with thyroid-specific expression of oncogenic BRAF (Tg-Braf) develop papillary thyroid cancers (PTC) that are locally invasive and have well-defined foci of poorly differentiated thyroid carcinoma (PDTC). To investigate the PTC-PDTC progression, we performed a microarray analysis using RNA from paired samples of PDTC and PTC collected from the same animals by laser capture microdissection. Analysis of 8 paired samples revealed a profound deregulation of genes involved in cell adhesion and intracellular junctions, with changes consistent with an epithelial-mesenchymal transition (EMT). This was confirmed by IHC, as vimentin expression was increased and E-cadherin lost in PDTC compared to adjacent PTC. Moreover, PDTC stained positively for phospho-Smad2, suggesting a role for transforming growth factor-beta (TGFbeta) in mediating this process. Accordingly, TGFbeta induced EMT in primary cultures of thyroid cells from Tg-Braf mice, whereas wild-type thyroid cells retained their epithelial features. TGFbeta-induced Smad2 phosphorylation, transcriptional activity and induction of EMT required MAPK pathway activation in Tg-Braf thyrocytes. Hence, tumor initiation by oncogenic BRAF renders thyroid cells susceptible to TGFbeta-induced EMT, through a MAPK-dependent process.
2011-03-23 | GSE27668 | GEO
Project description:Long noncoding RNAs (lncRNAs) have been shown to play a significant role in cancer biology. The aim of this study was to determine roles of lncRNAs in differences of clinical features related to the of papillary thyroid carcinoma (PTC) patients with or without Hashimoto's thyroiditis (HT). In the present study, we detected the differentially expressed lncRNAs in tumor tissues of PTC with or without HT by lncRNA microarrays. qRT-PCR, cell viability assay, cell cycle analysis and bioinformatics tools were used to verify and analyze the data. We found that 1031 lncRNAs and 1338 mRNAs were abnormally expressed in 10 tissue samples of PTC complicated with HT compared to pure PTC. Gene Ontology and pathway analyses of the mRNAs suggested that several biological processes and pathways, especially immune system processes, were promoted in PTC complicated with HT. Twenty lncRNAs were verified in 31 PTC complicated with HT and 64 pure PTC specimens using qRT-PCR, and the results were consistent with the microarrays data. Specifically, ENST00000452578, a down-regulated lncRNA in PTC complicated with HT, was negatively correlated with tumor size. Cell viability assay revealed that ENST00000452578 could inhibit cell proliferation. Co-expression analysis revealed that PPM1H, an mRNA regulated by ENST00000452578, may play an important role in cell cycle arrest. Our results indicate that lncRNAs and mRNAs plays an important role in the different clinical characteristics of PTC patients with or without HT, which might provide new insight from the perspective of RNA into the understanding of the cancers.
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