Project description:Molecular subtypes of SCLC have been defined by the expression status of ASCL1, NEUROD1, YAP1, and POU2F3 transcription regulators. ASCL1 knockdown resulted in decreased and increased expression of miR-375 and miR-455-3p, respectively. Analyses of publicly available transcriptome datasets suggested that miR-375 induced by ASCL1 is involved in YAP1 suppression whereas miR-455-3p is higher in non-neuroendocrine SCLC cells lacking ASCL1 expression.
Project description:ASCL1 is a master transcription factor for neuroendocrine differentiation. RNA-sequencing analysis on VMRC-LCD cells following ASCL1 knockdown revealed a subset of genes possibly regulated by ASCL1.
Project description:Molecular subtypes of SCLC have been defined by the expression status of ASCL1, NEUROD1, YAP1, and POU2F3 transcription regulators. ASCL1 knockdown resulted in decreased and increased expression of miR-375 and miR-455-3p, respectively. Analyses of publicly available transcriptome datasets suggested that miR-375 induced by ASCL1 is involved in YAP1 suppression whereas miR-455-3p is higher in non-neuroendocrine SCLC cells lacking ASCL1 expression.
Project description:To investigate the function of ASCL1 in ASCL1-positive lung adenocarcinoma, we established VMRC-LCD cell line in which the target gene has been knocked down by siRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different cells.
Project description:Ascl1 is a master transcription factor for neuroendocrine differentiation. RNA-sequencing analysis on CMT64 cells transduced with Ascl1 revealed a subset of genes possibly regulated by Ascl1.
Project description:ChIP-seq analysis was performed in an neuroblastoma cell line to analyze DNA bindings of H3K27ac in GI-MEN DOX-ASCL1 cells and ASCL1-HA in GI-MEN DOX-ASCL1-tag-HA cells.