Ontology highlight
ABSTRACT:
PROVIDER: PRJNA648039 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12301583_1.fastq.gz | Fastqsanger.gz | |||
| SRR12301583_2.fastq.gz | Fastqsanger.gz | |||
| SRR12301584_1.fastq.gz | Fastqsanger.gz | |||
| SRR12301584_2.fastq.gz | Fastqsanger.gz | |||
| SRR12301585_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
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Project description:Odontogenic tumors (OGTs), which originate from cells of odontogenic apparatus and their remnants, are rare entities. Primary intraosseous carcinoma, NOS (PIOC), is one of the OGTs, but it is even rarer and has a worse prognosis. The characteristics of PIOC, especially in immunohistochemical features and its pathogenesis, remain unclear. We characterized a case of PIOC arising from the left mandible, in which histopathological findings showed a transition between the odontogenic keratocyst and the carcinoma. The tumorous lesion of this PIOC exhibited malignant potentials with an invasive growth of carcinoma cells into the bone tissue, an elevated Ki-67 index, and lower signal for CK13 and higher signal for CK17 compared with the non-tumor region, histopathologically and immunohistopathologically. Further immunohistochemical analyses demonstrated increased expression of ADP-ribosylation factor (ARF)-like 4c (ARL4C) (accompanying expression of β-catenin in the nucleus) and yes-associated protein (YAP) in the tumorous lesion. On the other hand, YAP was expressed and the expression of ARL4C was hardly detected in the non-tumor region. In addition, quantitative RT-PCR analysis using RNAs and dot blot analysis using genomic DNA showed the activation of Wnt/β-catenin signaling and epigenetic alterations, such as an increase of 5mC levels and a decrease of 5hmC levels, in the tumorous lesion. A DNA microarray and gene ontology analysis demonstrated that numerous gene expression variations and signal activation, including Notch signaling, were altered in non-tumor and tumor lesions within this PIOC. Experiments with the GSK-3 inhibitor revealed that β-catenin pathway increased not only mRNA levels of ankyrin repeat domain1 (ANKRD1) but also protein levels of YAP and TAZ in oral squamous cell carcinoma cell lines. These results suggested that further activation of YAP signaling by Wnt/β-catenin signaling may be associated with the development of PIOC arising from odontogenic keratocyst in which YAP signaling is activated.
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Project description:Identification of beta-catenin interacting proteins via affinity purification with anti-beta-catenin antibody or IgG control in BCR-ABL1 transformed murine pre-B cells with induced beta-catenin activation via CTNNB1 exon3 fl/fl + Cre.
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Project description:Identification of beta-catenin interacting proteins via affinity purification with anti-beta-catenin antibody or IgG control in BCR-ABL1 transformed murine pre-B cells with induced beta-catenin activation via CTNNB1 exon3 fl/fl + Cre.
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Project description:Because of its insensitivity to existing radiotherapy, namely chemotherapy and targeted treatments, triple-negative breast cancer (TNBC) remains a great challenge to overcome. Increasing evidence has indicated abnormal Wnt/β-catenin pathway activation in TNBC but not luminal or HER2+ breast cancer, and lncRNAs play a key role in a variety of cancers. Through lncRNA microarray profiling between activated and inactivated wnt/β-catenin pathway of TNBC tissues, lnc-WAL (wnt/β-catenin associated lncRNA; WAL) was selected as the top upregulated lncRNA in wnt/β-catenin pathway activation compared with the inactivation group. RIP-seq was used to compare the β-catenin and IgG groups, where lnc-WAL could interact with β-catenin. Clinically, increased lnc-WAL in TNBC tumor tissue was associated with shorter survival. lnc-WAL promoted EMT, the proliferation, migration and invasion of breast cancer stem cells (BCSCs), and TNBC cells. Mechanistically, lnc-WAL inhibited β-catenin protein degradation via Axin-mediated phosphorylation at serine 45. Subsequently, β-catenin accumulated in the nucleus and activated the target genes. Importantly, wnt/β-catenin pathway activation stimulated the transcription of lnc-WAL. These results pointed to a master regulatory role of lnc-WAL/Axin/β-catenin in the malignant progression of TNBC. Our findings provide important clinical translational evidence that lnc-WAL may be a potential therapeutic target against TNBC.
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Project description:Diabetic cardiomyopathy (DCM) is a major complication of diabetes mellitus. Excessive activation of the canonical Wnt/β-catenin pathway contributes to the development of cardiomyopathy in type 1 diabetes mellitus (T1DM). Transcription factor 7-like 2 (TCF7L2) is the main β-catenin partner of the TCF family in adult human hearts. In this study, we investigated the role of Wnt/β-catenin in the development of cardiomyopathy in type 2 diabetes mellitus (T2DM) by using streptozotocin (STZ)/high-fat diet (HFD)-induced diabetic mice and high glucose-stimulated neonatal rat cardiomyocytes (NRCMs) as in-vivo and in-vitro models of T2DM, respectively. Compared with the control mice, the T2DM mice exhibited increased myocardial β-catenin and TCF7L2 expression that was concentrated in the nucleus. Treatment of diabetic mice with the β-catenin/TCF7L2 bipartite inhibitor iCRT14 prevented myocardial remodeling and improved cardiac dysfunction. iCRT14 also prevented high glucose-induced hypertrophy in NRCMs, while the β-catenin stabilizer SKL2001 worsened hypertrophy. Immunoprecipitation experiments confirmed the formation of the β-catenin/TCF7L2 bipartite in the control and T2DM mouse cardiomyocytes. Moreover, carbonic anhydrase 2 (CA2) was upregulated in T2DM cardiomyocytes in vitro and in vivo. TCF7L2 overexpression upregulated CA2, while iCRT14 treatment or TCF7L2 knockdown downregulated CA2. Chromatin immunoprecipitation (ChIP) experiments revealed an increased interaction between β-catenin/TCF7L2 and the transcription initiation region of CA2 in the heart tissue of T2DM mice. CA2 knockdown ameliorated NRCM hypertrophy induced by high glucose and SKL2001. A luciferase reporter assay confirmed that CA2 is directly regulated by the β-catenin/TCF7L2 bipartite. Collectively, these results indicate that the canonical Wnt/β-catenin pathway upregulates CA2 via TCF7L2 to promote cardiomyopathy in T2DM. This research sheds new light on the pathogenesis of DCM and presents new potential therapeutic targets for this disease.
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