Project description:We have identified TEAD4 as a key prognosis factor in colorectal cancer. To elucidate the potentail mechanism and function of TEAD4 in colorectal caner, we generated two stable cell lines expressing different shRNA targeting TEAD4 in the mesenchymal-like LoVo cells and the differential genes were detected by microarray. LoVo colorectal cancer cells stably expressing pLKO.1 control shRNA or sh1_shTEAD4 or sh2_shTEAD4
Project description:We have identified TEAD4 as a key prognosis factor in colorectal cancer. To elucidate the potentail mechanism and function of TEAD4 in colorectal caner, we generated two stable cell lines expressing different shRNA targeting TEAD4 in the mesenchymal-like LoVo cells and the differential genes were detected by microarray.
Project description:Transcription factor TEAD4 is overexpressed in CRC. To explore the potential new pro-tumorigenic function of TEAD4 in CRC, we performed RNA-seq analysis to identify new target genes of TEAD4 in HCT116 and SW620 cells
Project description:The TEAD (1-4) transcription factors comprise the conserved TEA/ATTS DNA binding domain recognising the MCAT element in the promoters of muscle-specific genes. Despite extensive genetic analysis, the function of TEAD factors in muscle differentiation has proved elusive due to redundancy amongst the family members. Expression of the TEA/ATTS DNA binding domain that acts a dominant negative repressor of TEAD factors in C2C12 myoblasts inhibits their differentiation, while selective shRNA knockdown of TEAD4 results in abnormal differentiation characterised by the formation of shortened myotubes. Chromatin immunoprecipitation coupled to array hybridisation (ChIP-chip) shows that TEAD4 occupies 867 promoters including those of myogenic miRNAs. We show that TEAD factors cooperate with MYOD1 to directly induce Myogenin, CDKN1A and Caveolin 3 expression to promote myoblast differentiation and fusion. RNA-seq identifies a novel set of TEAD4 target genes encoding muscle structural and regulatory proteins and those required for the unfolded protein response. In contrast, TEAD4 represses expression of the growth factor CTGF and Cyclin D1 to promote differentiation. Together these results show that TEAD factor activity is essential for C2C12 cell differentiation and define a novel and nonredundant role for TEAD4 in regulating the unfolded protein response. C2C12 cells were infected with retrotiviral vector expressing Flag-HA-Tagged TEAD4 or with empty control vector and selected in the continouos presence of puromycin. Infected cell populations were then differentiated for 5 days in DMEM medium with 2% horse serum and fixed in 0.4% formaldehyde.