TGFBR3 inhibits the aggressive of papillary thyroid cancer by inhibiting PI3K/AKT pathway and EMT
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1104217 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28796544_1.fastq.gz | Fastqsanger.gz | |||
| SRR28796544_2.fastq.gz | Fastqsanger.gz | |||
| SRR28796545_1.fastq.gz | Fastqsanger.gz | |||
| SRR28796545_2.fastq.gz | Fastqsanger.gz | |||
| SRR28796546_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Transforming Growth Factor Beta Receptor III (TGFBR3) had been shown to play a tumor suppressor role in a variety of cancers. However, its role in papillary thyroid cancer (PTC) remains a mystery. The purpose of this study was to determine the molecular mechanism and biological behavior of TGFBR3 in PTC, to further explore the regulatory pathway involved in TGFBR3 on PTC and provide potential targets for the diagnosis and treatment of invasive PTC.
2024-05-18 | GSE265794 | GEO
Project description:Non-small cell lung cancer (NSCLC) is a disease with high morbidity and mortality worldwide. NSCLC has significant metastasis ability, which is reported to be promoted by the process of epithelial-mesenchymal transition (EMT). The total flavonoid aglycone extract (TFAE) isolated from Scutellaria baicalensis was reported to inhibit tumor growth and induce cell apoptosis. Here we reconstructed TFAE (reTFAE) according to the main active components and revealed new mechanism in inhibiting EMT process of lung cancer. We provided the solid evidence that the compound mainly composed of baicalein, wogonin, and oroxylin-A presented inhibitory effect on the EMT process of A549 cells, and established the relationship between reTFAE, PI3K/Akt signaling pathways, TWIST1, and glycolysis pathway. The new mechanism we revealed and the new combination of research technologies including bioinformatics technology, chemical biology and molecular biology in our manuscript may be of tremendous interest to a broad range of academic, clinic and industrial researchers.
2022-01-25 | PXD030097 | Pride
Project description:Neuroblastoma is a pediatric tumor of the peripheral sympathetic nervous system with a highly variable prognosis. Activation of the PI3K/AKT pathway in neuroblastoma is correlated with poor patient prognosis, but the precise downstream effectors mediating this effect have not been determined. Here, we identify the forkhead transcription factor FOXO3a as a key target of the PI3K/AKT pathway in neuroblastoma. FOXO3a expression was elevated in low stage neuroblastoma tumors and normal embryonal neuroblasts, but reduced in late stage neuroblastoma. Inactivation of FOXO3a by AKT was essential for neuroblastoma cell survival. Treatment of neuroblastoma cells with the dual PI3K/mTOR inhibitor PI-103 activated FOXO3a and triggered apoptosis. This effect was rescued by FOXO3a silencing. Conversely, apoptosis induced by PI-103 or the AKT inhibitor MK-2206 was potentiated by FOXO3a overexpression. Further, levels of total or phosphorylated FOXO3a correlated closely with apoptotic sensitivity to MK-2206. In clinical specimens, there was an inverse relationship between gene expression signatures regulated by PI3K signaling and FOXO3a transcriptional activity. Moreover, high PI3K activity and low FOXO3a activity were each associated with an extremely poor prognosis. Our work indicates that expression of FOXO3a and its targets offer useful prognostic markers as well as biomarkers for PI3K/AKT inhibitor efficacy in neuroblastoma. Affymetrix U133 Plus 2.0 profiling of SY5Y-TetR-FOXO3A cells treated with doxycycline and/or the PI3K/mTOR inhibitor PI-103. Each condition profiled in triplicate.
2013-05-01 | E-GEOD-42762 | biostudies-arrayexpress
Project description:EZH2 upregulates the PI3K/AKT pathway through IGF1R and MYC in clinically aggressive CLL
| PRJNA475984 | ENA
Project description:Papillary craniopharyngiomas (PCPs) are biologically benign but clinically aggressive lesions hence affect the quality of life. The expression of inflammatory mediators and regulation of the immune microenvironment in PCPs have not been investigated much. In this study, for the first time, we assessed the immune cell infiltration and immune cell signatures in PCPs by analyzing the bulk-RNA sequencing data. Our results indicated that PCPs are in a state of high immune infiltration but low action with abundant inflammatory cells.
2022-10-28 | GSE216330 | GEO
Project description:Immune Infiltration in Aggressive Papillary Craniopharyngioma: High infiltration But Low Action
| PRJNA892989 | ENA
Project description:Neuroblastoma is a pediatric tumor of the peripheral sympathetic nervous system with a highly variable prognosis. Activation of the PI3K/AKT pathway in neuroblastoma is correlated with poor patient prognosis, but the precise downstream effectors mediating this effect have not been determined. Here, we identify the forkhead transcription factor FOXO3a as a key target of the PI3K/AKT pathway in neuroblastoma. FOXO3a expression was elevated in low stage neuroblastoma tumors and normal embryonal neuroblasts, but reduced in late stage neuroblastoma. Inactivation of FOXO3a by AKT was essential for neuroblastoma cell survival. Treatment of neuroblastoma cells with the dual PI3K/mTOR inhibitor PI-103 activated FOXO3a and triggered apoptosis. This effect was rescued by FOXO3a silencing. Conversely, apoptosis induced by PI-103 or the AKT inhibitor MK-2206 was potentiated by FOXO3a overexpression. Further, levels of total or phosphorylated FOXO3a correlated closely with apoptotic sensitivity to MK-2206. In clinical specimens, there was an inverse relationship between gene expression signatures regulated by PI3K signaling and FOXO3a transcriptional activity. Moreover, high PI3K activity and low FOXO3a activity were each associated with an extremely poor prognosis. Our work indicates that expression of FOXO3a and its targets offer useful prognostic markers as well as biomarkers for PI3K/AKT inhibitor efficacy in neuroblastoma.
2013-05-01 | GSE42762 | GEO
Project description:BackgroundTransforming growth factor beta receptor III (TGFBR3) has been shown to play a tumor-suppressive role in a variety of cancers. However, its role in papillary thyroid cancer (PTC) remains unknown.MethodTGFBR3 expression levels in PTC were analyzed utilizing The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Edu, wound healing, and Transwell assays were used to evaluate cell proliferation, migration, and invasion. Transcriptome sequencing, quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR), and Western blotting were used to detect the underlying mechanism of TGFBR3 in PTC progression.ResultThis study demonstrated that TGFBR3 expression was significantly down-regulated in PTC compared to normal thyroid tissues. Low expression of TGFBR3 was associated with poor prognosis of patients with PTC. Furthermore, TGFBR3 expression positively correlated with thyroid differentiation score. In investigating the biological impact of TGFBR3 overexpression in PTC cell lines, we found that the proliferation, migration, and invasion of PTC cells were significantly inhibited in response to TGFBR3 overexpression. Moreover, we also demonstrated that overexpression of TGFBR3 inhibited the PI3K/AKT pathway and epithelial-mesenchymal transformation processes. Lastly, TGFBR3 expression was found to be involved in tumor immune infiltration, highlighting its potential influence on immune dynamics within the tumor microenvironment in PTC.ConclusionTGFBR3 plays a tumor-suppressive role in PTC progression by inhibiting the PI3K/AKT pathway and epithelial mesenchymal transformation.
| S-EPMC11623029 | biostudies-literature
Project description:Epithelial/mesenchymal transition (EMT) is associated with loss of cell adhesion molecules, such as E-cadherin, and increased invasion, migration, and proliferation in epithelial cancers. In non-small cell lung cancer (NSCLC), EMT is associated with greater resistance to EGFR inhibitors. However, its potential to predict response to other targeted drugs or chemotherapy has not been well characterized. The goal of this study was to develop a robust, platform-independent EMT gene expression signature and to investigate the association of EMT and drug response in NSCLC. A 76-gene EMT signature was derived in 54 DNA-fingerprinted NSCLC cell lines and tested in an independent set of cell lines and in NSCLC patients from the BATTLE clinical trial. The signature classified cell lines as epithelial or mesenchymal independent of the microarray platform and correlated strongly with E-cadherin protein levels, as measured by reverse phase protein array. Higher protein expression of Rab25 (in epithelial lines) and Axl (in mesenchymal lines), two signature genes associated with in EMT in other cancer types, was also confirmed. Mesenchymal cell lines demonstrated significantly greater resistance to EGFR inhibition, independent of EGFR mutation status and were more resistant to drugs targeting the PI3K/Akt pathway. We observed no association between EMT and response to cytotoxic chemotherapies, including cisplatin, pemetrexed, and docetaxel monotherapy and/or doublets (p-values ≥0.2). In NSCLC patients, the EMT signature predicted 8-week disease control in the erlotinib arm, but not in other treatment arms. In conclusion, we have developed a robust EMT signature that predicts resistance to EGFR inhibitors and PI3K/Akt pathway inhibitors. Gene expression profiles were measured in 131 core biopsies from patients with refractory non-small cell lung cancer in the Biomarker-integrated Approaches of Targeted Therapy for Lung Cancer Elimination (BATTLE) trial. We used the BATTLE dataset to test an EMT gene expression signature trained in cell lines and independant of the microarray platform.
2012-10-25 | E-GEOD-33072 | biostudies-arrayexpress
Project description:miRNA expression profiles in non-aggressive, invasive and metastatic papillary thyroid cancer
| PRJNA533088 | ENA