Similar Datasets
Project description:CHI3L1 regulates papillary thyroid tumor progression via TP53 signaling
| PRJNA1204810 | ENA
Project description:Genome-wide gene expression analysis in TPC-1 cells transfected with and without expression construct for PTCSC3 . TPC-1 cells were transiently transfected in quadruplicate with an empty vector (pcDNA3) and with the expression vector harboring cDNA for PTCSC3. After 24 hours from transfection total RNA was extracted and used for microarray expreiment.
2012-04-30 | E-GEOD-32195 | biostudies-arrayexpress
Project description:Genome-wide gene expression analysis in TPC-1 cells transfected with and without expression construct for PTCSC3 .
2012-05-01 | GSE32195 | GEO
Project description:To investigate the short-termed and long-termed transcriptomic changes induced by the RET tyrosine kinase inhibitor BLU667 in TPC-1 human PTC cells
2023-04-11 | GSE211371 | GEO
Project description:Papillary thyroid cancer (PTC) is the most prevalent type of TC worldwide; however, its pathological process remains unclear at the molecular level. In the current study, we analyzed the microarray data of PTC tissues and non-neoplastic thyroid tissues, and confirmed miR-100-5p as a downregulated miRNA in PTC. Via bioinformatic approach, western blotting, and TOP/FOP-flash assay, miR-100-5p was observed to be involved in the inactivation of Wnt/β-catenin signaling in TPC-1 and KTC-1. Frizzled Class Receptor 8 (FZD8), the coupled receptor for canonical Wnt/β-catenin signaling, was verified to be targeted and inhibited by miR-100-5p in TPC-1 and KTC-1. In the function assay, miR-100-5p mimic repressed PTC cell proliferation and induced cell apoptosis of TPC-1 and KTC-1; meanwhile, transfection of full-length FZD8 attenuated the effect of miR-100-5p mimic. Moreover, in the collected samples, miR-100-5p was lowly expressed in PTC tissues compared with normal tissues, especially in those of advanced stage (Stage III/IV vs Stage I/II), while FZD8 was highly expressed in PTC tissues, which in PTC tissues was inversely correlated to miR-100-5p. Thus, we suggest that overexpression of miR-100-5p inhibits the development of PTC by targeting FZD8.
| S-EPMC9263890 | biostudies-literature
Project description:The incidence of papillary thyroid cancer (PTC) has been steadily rising, though the underlying mechanism remains unclear. This study aims to elucidate the biological role of TM4SF4 in the PTC progression. Our differential expression analysis indicated that TM4SF4 was significantly upregulated in PTC, which was corroborated in both our local cohort and the data from Human Protein Atlas. Additionally, clinical characteristics analysis and receiver operating characteristic curves (ROC) demonstrated that TM4SF4 served as a significant diagnostic marker for PTC. Correlation and enrichment analysis of TM4SF4-related partners suggested that it was involved in cell junction and cohesion processes. Furthermore, immune infiltration analysis revealed a positive correlation between TM4SF4 expression and the immune activation in PTC. Importantly, in vitro experiments demonstrated that TM4SF4 downregulation suppressed the proliferation and metastasis of PTC cell lines while inducing apoptosis. We further discovered that the AKT activator SC79 was able to reverse the malignant behaviors suppression caused by TM4SF4 knockdown, suggesting that TM4SF4 may promote PTC progression via the AKT pathway. In conclusion, our study highlights the oncogenic role of TM4SF4 in PTC and identifies it as a novel biomarker for diagnosis and treatment.
| S-EPMC11540099 | biostudies-literature
Project description:MiR-324-5p is overexpressed in papillary thyroid carcinoma (PTC) with lymph node metastasis and promotes malignant phenotypes of KTC-1 cell line. However, the detailed regulatory mechanism remains unknown. Tumor microenvironment plays a key role in tumor progression. CCAAT enhancer-binding protein delta (CEBPD) is important in immune and inflammatory responses. In this study, we investigated the interaction between miR-324-5p/PTPRD/CEBPD axis and tumor microenvironment in PTC progression. K1 and KTC-1 were transfected by lenti-CEBPD or CEBPD-sh vectors. Supernatant from different groups was harvested and added into culture media of human macrophages and HUVEC. Cell viability, colony formation, invasive and migrated cell number, and gap closure rate were elevated in lenti-CEBPD group. Compared with the control, supernatant from lenti-CEBPD group contained more abundant levels of VEGF and IL-4/IL-13, which, respectively, induced higher HUVEC invasion/migration rates and more obvious M2 marker (CD206) and genes (PPAR-γ and MRC-1) expression in macrophages. By means of luciferase reporter assay and gene manipulation, we identified that CEBPD was negatively regulated in PTC by protein tyrosine phosphatase receptor delta (PTPRD) which was the target of miR-324-5p. CEBPD-shRNA was also proved to reverse the effect of PTPRD-sh1 or miR-324-5p mimic on IL-4/IL-13 expression and HUVEC invasion. These results suggested that miR-324-5p/PTPRD/CEBPD axis was involved in the progression of PTC by inducing HUVEC invasion/migration and macrophage M2 polarization via VEGF and IL4/IL13, respectively.
| S-EPMC7515492 | biostudies-literature
Project description:Background：In present study, we aimed to evaluate the level as well as function of circulating MDSCs in papillary thyroid cancer (PTC), and also explore the underlying mechanism of MDSCs during tumor progression. Methods：microRNA arrays and RNA-seq analysis were conducted to screened out differentially expressed miRNAs and mRNAs between TPC-1 cells cocultured with PMN-MDSCs and untreated TPC-1 cell line. Results：19 miRNAs were differentially expressed, of which 10 were downregulated and 9 were upregulated in MDSC-conditioned cancer cells. GO analysis of miRNA predicted target genes showed that inflammatory related response were enriched. Besides, these genes were mainly related to NF-kappa B, PI3K-AKT and TNF signaling pathways which are associated with immune response as well as cancer development by KEGG pathway analysis. For validation, qRT-PCR was used to assess the differentially expressed miRNA and the trends in the expression was consistent between microRNA-seq and qRT-PCR. Conclusion：Collectively, our work explore the mechanism by which PMN-MDSCs paly a critical role in PTC
2019-11-08 | GSE140109 | GEO
Project description:Background: Tumor-associated calcium signal transducer 2 (TROP2) is over expressed in various kinds of human cancers and plays important roles in the proliferation, invasion and metastasis of tumor cells. However, the expression and molecular mechanism of TROP2 in thyroid papillary carcinoma (PTC) are unclear. Methods: The expressions of TROP2 in PTC and control tissue were detected by real-time reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. The proliferation and invasion of PTC cell lines were examined by cell cloning and transwell assays. RNA sequencing analysis and public data analysis were assessed to investigate the potential mechanisms of TROP2 in PTC. Gene correlation analysis was conducted to explore the association between TROP2 and the related gene ISG15 in patients with PTC. Results: The expression of TROP2 was significantly higher in PTC than control. The high expression of TROP2 protein was associated with lymph node metastasis, tumor size and capsular infiltration (P<0.05). SiRNA-mediated TROP2 gene expression silencing can significantly inhibit proliferation and migration of PTC cells. ISG15 decreased in TROP2 siRNA PTC cells and increased in PTC patients significantly. There was a significant correlation between the expression of TROP2 and ISG15 in PTC patients. TROP2 interacted directly with ATP6V1A, CEBPA and SOX5 and then further interacted with the immune genes. TROP2 expression and tumor-infiltrating immune cells were also correlated in thyroid cancer microenvironment. Conclusions: TROP2 promotes the development of PTC. TROP2 expression was correlated with ISG15 and tumor-infiltrating immune cells in thyroid cancer.
| S-EPMC8518010 | biostudies-literature
Project description:BackgroundThe incidence and mortality of thyroid cancer (TC) has been steadily rising in the past decades. It is imperative to have a better understanding of the molecular mechanisms underlying TC development and identify novel therapeutic targets. This study characterized the role of lncRNA CALML3-AS1 (CALML3-AS1) in the development of papillary thyroid cancer (PTC).MethodRelated mRNAs expression were validated in the tumor and adjacent normal tissues from 52 PTC patients and PTC cell lines by qRT-PCR. Expression of RBM38 was detected by Western blot. We have also conducted CCK-8 and colony formation assays were used to detect the effect of CALML3-AS1 on cell proliferation, Transwell assay was utilized to evaluate cell migration and invasion, apoptosis detected by flow cytometry assay, RNA pull-down and luciferase assays were performed to validate gene predictions.ResultsThe results indicated that the expression of both CALML3A-S1 and RBM38 were significantly downregulated in PTC tissues (p < 0.01), while the expression of miR-20a-5p was increased in PTC (p < 0.01). Functionally, CALML3-AS1 overexpression inhibited PTC cell proliferation in vitro and in vivo. Mechanistically, CALML 3-AS1 sponged miR-20a-5p, which in turn leads to the suppression of RBM38 expression and PTC progression.ConclusionsCALML3-AS1 functions as a ceRNA for miR-20a-5p in the regulation of the expression of RBM38 in PTC. Higher level of CALML3-AS1 serves as a good prognostic indicator of survival in PTC patients. Targeting CALML3-AS1/ miR-20a-5p/RBM38 axis may represent a novel therapeutic strategy in the treatment of PTC.
| S-EPMC8966157 | biostudies-literature