Project description:Analysis of the effect of TNFα on the expression of lncRNA during EPO or GM-CSF culture, in TF-1 cells at different time points. The study attemps to determine the differents keys lncRNA Regulating response or regulated by TNFα during EPO induced differentiation or basal culture with GM-CSF.
Project description:The experiment aims to distinguish the transcriptome influenced by the extinction of the lncRNA, after treatment with TNF_ with or without PPTG1-1:1 extinction.
Project description:Interventions: Colorectal cancer surgery
inguinal hernia surgery
Primary outcome(s): TNF-a expression by myeloid cells in ascites
Study Design: Parallel Non-randomized
Project description:Acute myeloid leukemia (AML) is a hematologic malignancy with a poor prognosis. We discovered that BMAL1 is a ferroptosis suppressor. Furthermore, it was also found to be overexpressed in AML patients, affecting the cell cycle and promoting tumor cell growth and progression. In this study, we further validated the association of BMAL1 with the progression and survival outcomes of AML. Lipidomic revealed that the levels of ceramide increased in AML cells following the depletion of BMAL1. Ceramide facilitated ferroptosis in AML cells. ASAH2 played a key role in this process. BMAL1 could not directly regulate ASAH2 but instead through IKZF2. Elevated levels of ceramide promoted the degradation of the ferroptosis protection molecule GPX4, ultimately promoting ferroptosis. Furthermore, ceramide treatment has been demonstrated to enhance the responsiveness of AML cells to sorafenib. In summary, this study elucidates that BMAL1 depletion remodels ceramide metabolism to regulate the sensitivity of AML cells to ferroptosis and targeted drug sorafenib.
Project description:In this work we dissect the functional role of the HOXB-AS3 long non coding RNA in patients with NPM1-mutated (NPM1mut) acute myeloid leukemia (AML). We show that HOXB-AS3 regulates the proliferative capacity of NPM1mut AML blasts in vitro and in vivo. HOXB-AS3 was found to interact with the ErbB3-binding protein 1 (EBP1) and guide EBP1 to the ribosomal DNA locus. Via this mechanism HOXB-AS3 regulates ribosomal RNA transcription and de novo protein synthesis. We propose that in the context of NPM1 mutations, HOXB-AS3 overexpression acts as a compensatory mechanism, which allows adequate protein production in leukemic blasts.
Project description:DA and congenic R11 macrophages were stimulated with zymosan for 1 or 24 hours and pro-inflammatory mediators measured at mRNA level R11 macrophages had reduced pro-inflammatory mediators after stimulation