Ontology highlight
ABSTRACT:
PROVIDER: PRJNA243278 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptome was assessed in the transitions from the normal thymus (with regular progenitor turnover), to a thymus devoid of extrinsic progenitor competition for 10 weeks, to fully malignant T cell acute lymphoblastic leukemia (T-ALL). Comparison of global gene expression between normal thymus, to thymus grafts with autonomous thymopoiesis, and T-ALL
2014-05-16 | E-GEOD-56417 | biostudies-arrayexpress
Project description:Transcriptome was assessed in the transitions from the normal thymus (with regular progenitor turnover), to a thymus devoid of extrinsic progenitor competition for 10 weeks, to fully malignant T cell acute lymphoblastic leukemia (T-ALL).
2014-05-16 | GSE56417 | GEO
Project description:Two major genetic pathways leading to colorectal carcinoma can well be distinguished; the ‘suppressor pathway’, which is characterized by inactivation of tumor-suppressor genes and the ‘mutator pathway’, which is characterized by microsatellite instability. The purpose of this study is to explore a third putative pathway; microsatellite and chromosome stable colorectal cancer where an alternative cancer-causative mechanism might play a role.
| 2021019 | ecrin-mdr-crc
Project description:Tumor-Derived G-CSF Facilitates Neoplastic Growth through a Granulocytic Myeloid-Derived Suppressor Cell-Dependent Mechanism
| PRJNA147477 | ENA
Project description:Aberrant activation of RAS/MAPK signaling is a driver of over one third of all human carcinomas. The homologous transcription factors ETS1 and ETS2 mediate the activation of gene expression programs downstream of RAS/MAPK signaling. ETS1 is important for oncogenesis in many tumor types. However, ETS2 can act as an oncogene in some cellular backgrounds, and as a tumor suppressor in others, and the molecular mechanism responsible for this cell-type specific function remains unknown. Here, we show that ETS1 and ETS2 regulate a cell migration gene expression program in opposite directions, and provide the first comparison of the ETS1 and ETS2 cistromes. This genomic data, and an ETS1 deletion line are used to show that the opposite function of ETS2 is due to binding site competition and a weaker activation function of ETS2 compared to ETS1. This weaker activation was mapped to the ETS2 N-terminus and a specific interaction with the co-repressor BS69 (ZMYND11). Gene expression data from tumor cohorts was then used to show that BS69 expression level in tumors correlates with oncogenic and tumor suppressive roles of ETS2. Therefore, these data indicate a novel and specific mechanism allowing ETS2 to switch between oncogenic and tumor suppressive functions in a cell-type specific manner.
2017-02-13 | GSE86238 | GEO
Project description:Expression data from mouse normal thymus, thymus tumor, and XIST resistant thymus tumor
| PRJNA111703 | ENA
Project description:Competition among RNAs to bind miRNA is proposed to influence biological systems. However, the role of this competition in disease onset is unclear. Here, we report that TYRP1 mRNA, in addition to encoding tyrosinase-related protein 1 (TYRP1), indirectly governs cell proliferation by sequestering miR-16 to non-canonical miRNA response elements (MREs). Consequently, the sequestered miR-16 is no longer able to repress its mRNA targets, such as RAB17, which is involved in melanoma cell proliferation and tumor growth. Restoration of miR-16 tumor suppressor function can be achieved in vitro by silencing TYRP1 or increasing miR-16 expression. Importantly, TYRP1-dependent miR-16 sequestration can also be overcome in vivo by using small oligonucleotides that mask miR-16 binding sites on the TYRP1 mRNA. Together, our findings assign a pathogenic noncoding function to the TYRP1 mRNA and highlight miRNA displacement as a new targeted therapeutic approach in melanoma.
2017-08-08 | GSE95589 | GEO
Project description:Although increasing studies have proved cell competition widely involved in the growth and homeostasis of multicellular organisms is closely linked to tumorigenesis and development, the mechanistic contributions between drug resistance and tumor cell competition remain ill-defined. In this paper, we applied MS of cell competition group to determine the dominant characteristics of lenvatinib resistance and its metabolic differences in cell competition. Our results showed a vital role of HSP90-IDH1 mediated lipid accumulation in maintaining the competitive outcome of HCC drug-resistant cells via regulating lipid metabolism. HSP90-IDH1 axis could be a promising target to overcome HCC drug resistance.
2023-10-20 | PXD046294 |
Project description:Stem cell quiescence acts as a tumor suppressor mechanism in hair follicle initiated squamous tumors
| PRJNA224969 | ENA
Project description:Stem Cell Quiescence acts as a tumor suppressor mechanism in hair follicle initiated squamous tumors
| PRJNA225583 | ENA