Project description:Colorectal cancer malignant progression depends on the aberrant oncogenic expressions. During tumorigenesis, the oncogeneic genes mutation or expression, following specific sets of genes are up-regulated or down-regulated. Some of them, for instance, control metabolism reprogramming to promote tumor growth and maliganant progression. We used microarrays to detail the global programme of gene expression regulated by ILF3, which is overexpressed in colorectal cancer.
Project description:Our data showed that lncRNA ELF3-AS1 could bind on the exon1 of ELF3-201 to form a double-stranded RNA molecule. This double-stranded RNA could interact with ILF2/ILF3 complex. To explore the biofunction of the interaction between ELF3-AS1 and ILF2/ILF3 complex, loss-of-function studies regarding ILF2 and ILF3 were performed in SGC7901 cell line. RNA sequencing studies showed that knockdown of ILF3 significantly decreased ELF3-AS1, while knockdown of ILF2 significantly increased ELF3-AS1 and NF90 expression. Our data revealed that ILF2/ILF3 complex interacted with ELF3-AS1/ELF3 double-stranded RNA and regulated their transcripts stability.
Project description:Knockdown of H19 leads to cell cycle arrest, reduced cell proliferation, and reduced cell migration in DLD1 cells. We used microarrays to detail the global programme of gene expression following H19 knockdown in DLD1 cells
Project description:DLD1 is an APC mut, KRAS mut, P53 mut CRC cell line. PROX1 transcription factor, target of Wnt pathway in CRC, is our protein of interest.DLD1 cells are PROX1 negative. We overexpressed through lentiviral expression PROX1 protein or the empty vector psd44, through selection of the cells in puromycin resistance. Afterwards we compared the transcriptional program of the DLD1-PROX1 and DLD1-Control cells growing in monolayer in vitro.
Project description:Antigen presenting cells such as myeloid dendritic cells (DCs) are key sentinels of the innate immune system. In response to pathogen recognition and innate immune stimulation, DCs transition from an immature, inactive state to a mature, active state that is characterized by widespread changes in host gene expression. Several key transcription factors are known to drive these gene expression changes, but the mechanisms that negatively regulate DC maturation are less well understood. Here, we have identified that the transcription factor Interleukin Enhancer Binding Factor 3 (ILF3) is a negative regulator of innate immune responses and DC maturation. Depletion of ILF3 in primary human monocyte-derived DCs (MDDCs) using shRNA knockdown led to increased expression of maturation markers and potentiated innate responses at baseline.
Project description:We overexpressed YAP-S127D in DLD1 colorectal cancer cells for 21 days after sub-cutaneous (SubQ) injection into the flanks of nude mice.
Project description:Small interfering RNA (siRNA) mediated depletion of Lamin A/C and Lamin B2 was performed in a diploid colorectal cancer cell line - DLD1 with an aim to identify transcription deregulation across the genome.
Project description:RNA pulldown assay showed that lncRNA UBE2CP3 could bind to ILF3 protein. In order to further verify the interaction between ILF3 and UBE2CP3, RNA Immunoprecipitation (RIP) assay was performed to identify the RNAs that binds to ILF3 protein. RIP-seq data verifies the interaction between ILF3 and UBE2CP3. Interestingly, UBE2CP3 could also binds to 3'UTR of IGFBP7 mRNA. Mechanismly, lncRNA UBE2CP3 and 3' UTR of IGFBP7 could forms an double-stranded RNA. Then, the RNA duplex could interact with the Double-Stranded RNA-Binding Protein ILF3.