Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA213615 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We examined the function of miR-150 in T-cell lymphomagenesis. We transfected GFP-control or GFP-miR-150 into several T-cell lymphoma lines and sought which genes were regulated by miR-150. To examine the function of miR-150 in T-cell lymphomagenesis, we first transfected GFP-control (Mock) or GFP-miR-150 into several T-cell lymphoma lines (ATN-1, HUT78, My-La, and HH). To detect genes commonly downregulated among these cells, we used the CodeLinkTM Human Whole Genome Bioarray platform with the criterion that the miR-150/GFP-control ratio must be <0.75 in all 3 CTCL lines.
2013-07-30 | E-GEOD-49308 | biostudies-arrayexpress
Project description:Increasing evidences support a potential role for the Signal Transducer and Activator of Transcription-3 (STAT3) as a tumor driver in cutaneous T-cell lymphoma (CTCL). However, the mechanisms leading to STAT3 pathway activation in CTCL and how STAT3 activation contributes to lymphomagenesis remains primarily not enough explored. Recently, we found that miR-124, a known STAT3 regulator in cancer, is robustly silenced in Mycosis Fungoides (MF) tumor-stage and CTCL cell lines and we have herein studied whether deregulation of miR-124 contributes to activate STAT3 pathway in CTCL. Material and Methods: DNA methylation status of miR-124 and its expression levels in response to the DNA-demethylating agent azacitidine were evaluated in CTCL cell lines by pyrosequencing analysis. CTCL cell lines were transient transfected with a lentiviral vector encoding miR-124 and transfected cells were analyzed for phosphorylated STAT3 (P-STAT3) levels. The impact on STAT3 signaling was evaluated using expression microarray on CTCL cell lines in both conditions, miR-124 absent (malignant condition) versus miR-124 expressed (lentiviral transduction). Results: A significant promoter methylation and silencing of miR-124 in MF tumor samples and CTCL cell lines was detected. DNA methylation levels of miR-124 in CTCL cell lines were restored (and subsequently miR-124 were overexpressed) after DNA demethylation. Ectopic lentiviral expression of miR-124 downregulated STAT3 in the different CTCL cell lines. Genes differentially expressed regarding miR-124 regulation in CTCL cell lines indicated impact on known cell survival and function pathways and, particularly, intervention on miR-124 expression modulated different STAT3 pathway components. Conclusions: Our study deciphers a novel epigenetic mechanisms regulating STAT3 pathway in CTCL. This might contribute to a better understanding the molecular basis in CTCL development. Deregulation of STAT3 seems to have a major impact on cell survival in CTCL cell lines indicating the potential interest of targeting STAT3 with specific therapies.
2020-12-31 | GSE130809 | GEO
Project description:We examined the function of miR-150 in T-cell lymphomagenesis. We transfected GFP-control or GFP-miR-150 into several T-cell lymphoma lines and sought which genes were regulated by miR-150.
2013-07-30 | GSE49308 | GEO
Project description:Adult T-cell leukemia (ATL) is a highly aggressive T-cell malignancy characterized by human T-cell leukemia virus type 1 (HTLV-1) infection. ATL has a very poor prognosis and lacks satisfactory treatments; therefore, it is critical to identify novel targets in ATL cells in order to develop effective targeted therapeutics. Here we report the identification of two novel oncogenes, AK4 and RHOC, as target genes of miR-455-3p, a tumor suppressive microRNA in ATL patients. Importantly, AK4 and RHOC are highly expressed in ATL and exhibit oncogenic potentials in vitro and in vivo. Interestingly, transcriptome and metabolome analyses reveal a functional overlap of AK4 and RHOC, including activating oncogenic pathways such as Myc targets and deregulating lipid metabolism such as enhancing the production of sphingomyelin, a tumor-promoting lipid. In particular, compared to other types of T-cell malignancy such as T-ALL and CTCL, ATL is sensitive to sphingomyelin inhibition and AK4 or RHOC depletion. Altogether, we report a distinct dependency of ATL on newly characterized oncogenes AK4 and RHOC and an oncometabolite sphingomyelin, which together represent novel targetable vulnerabilities of ATL that could be exploited for developing effective therapeutics.
2025-02-03 | MTBLS11858 | MetaboLights
Project description:Adult T-cell leukemia (ATL) is a highly aggressive T-cell malignancy characterized by human T-cell leukemia virus type 1 (HTLV-1) infection. ATL has a very poor prognosis and lacks satisfactory treatments; therefore, it is critical to identify novel targets in ATL cells in order to develop effective targeted therapeutics. Here we report the identification of two novel oncogenes, AK4 and RHOC, as target genes of miR-455-3p, a tumor suppressive microRNA in ATL patients. Importantly, AK4 and RHOC are highly expressed in ATL and exhibit oncogenic potentials in vitro and in vivo. Interestingly, transcriptome and metabolome analyses reveal a functional overlap of AK4 and RHOC, including activating oncogenic pathways such as Myc targets and deregulating lipid metabolism such as enhancing the production of sphingomyelin, a tumor-promoting lipid. In particular, compared to other types of T-cell malignancy such as T-ALL and CTCL, ATL is sensitive to sphingomyelin inhibition and AK4 or RHOC depletion. Altogether, we report a distinct dependency of ATL on newly characterized oncogenes AK4 and RHOC and an oncometabolite sphingomyelin, which together represent novel targetable vulnerabilities of ATL that could be exploited for developing effective therapeutics.
2025-02-03 | MTBLS11844 | MetaboLights
Project description:Transcriptional profiling controlled by PRKCQ of human CTCL cell lines MyLa and HuT 78 comparing cells transfected with non-targeting control with shPRKCQ cells at resting conditions and by TPA. The objective was to explore the role of PRKCQ in the pathogenesis of cutaneous T-cell lymphoma(CTCL).
2020-09-04 | GSE157442 | GEO
Project description:Cutaneous T cell lymphoma (CTCL) is characterized by the proliferation of CD4+ T cells in a background of chronic inflammation, where malignant CTCL cells escape immune surveillance and are not eliminated. To study how miRNAs (miRs) regulate T cell exhaustion in this disease, we performed miRseq analysis, qRT-PCR, and in situ hybridization on 45 primary CTCL samples, 3 healthy skin samples, and CTCL cell lines, identifying miR-155-5p, -130b-3p and -21-3p. Moreover, miR-155-5p, -130b-3p, and -21-3p positively correlated with immune checkpoint gene expression in lesional skin samples and were enriched in the IL6/JAK/STAT signaling pathway by gene set enrichment analysis.
2021-12-07 | GSE181118 | GEO
Project description:Restoring miR-150-5p to breast cancer cell lines
| PRJNA345308 | ENA
Project description:Cutaneous T-cell lymphomas (CTCL) are the most frequent primary skin lymphomas. Nevertheless, diagnosis of early disease has proven difficult due to a clinical and histological resemblance to benign inflammatory skin diseases. To address if microRNA (miRNA) profiling can discriminate CTCL from benign inflammation, we study miRNA expression in 199 patients with CTCL, peripheral T-cell lymphoma (PTL), and benign skin diseases (psoriasis and dermatitis). Using microarrays we show that the most induced- (miR-326, miR-663b, miR-711) and repressed- (miR-203, miR-205) miRNAs distinguish CTCL from benign skin diseases with > 90% accuracy in a training set of 90 samples and a test set of 58 blinded samples. These miRNAs also distinguish malignant and benign lesions in an independent set of 50 patients with PTL and skin inflammation and in experimental human xenograft mouse models of psoriasis and CTCL. Q-RT-PCR analysis of 104 patients with CTCL and benign skin disorders validates differential expression of 4 out of the 5 miRNAs and confirms previous reports on miR-155 in CTCL. A q-RT-PCR-based classifier consisting of miR-155, miR-203, and miR-205 distinguishes CTCL from benign disorders with high specificity, sensitivity, and a classification accuracy of 95% indicating that miRNAs have a high diagnostic potential in CTCL.
2011-11-22 | GSE31408 | GEO
Project description:Gene expression profiling in prostate cancer cell lines transfected with miR-33a
| PRJNA349984 | ENA