Project description:This SuperSeries is composed of the following subset Series: GSE30815: CDK8 knockdown in HT-29 human colon cancer cells GSE30816: CDK8 and MED12 knockdown in R1 mouse ES cells Refer to individual Series
Project description:Transcriptional profiling of HT-29 human colon cancer cells transfected with non-targeting control (NTC) siRNA and two different siRNA sequences against CDK8 (siCDK8-1 and siCDK8-2).
Project description:Transcriptional profiling of HT-29 human colon cancer cells transfected with non-targeting control (NTC) siRNA and two different siRNA sequences against CDK8 (siCDK8-1 and siCDK8-2). Three condition experiment comparing siNTC versus siCDK8-1 and siCDK8-2 after 3 days (3 biological replicates each); in total 9 samples profiled.
Project description:Purpose: Identify genes regulated by GPR126 in colon cancer cells by RNA-seq analysis Methods: Use shRNAs to knock down GPR126 in HT-29 cells, total RNAs from scramble group (NC) and GPR126 knockdown group (Sh1) were subjected to RNA-sequencing. Results: Around 700 transcriptomes were up-regulated in GPR126 knockdown HT-29 cells, and 14000 transcriptomes were down-regulated in GPR126 knockdown HT-29 cells.GPR126 mainly regualtes genes from DNA synthesis and cell cycle-related pathways. Conclusions: Our study firstly showed the function of GPR126 regulating colon cancer cell proliferation by targeting genes invovled in DNA synthesis and cell cycle-related pathways.
2017-11-09 | GSE106696 | GEO
Project description:CDK8 knockdown in HT-29 cells and CDK8 & MED12 knockdown in R1 cells
Project description:Achaete scute-like 2 (Ascl2), a basic helix-loop-helix (bHLH) transcription factor, controls the fate of intestinal stem cells. However, the role of Ascl2 in colon cancer progenitor cells remains unknown. The cell lines HT-29 (47.5-95% of CD133+ population) and LS174T (0.45% of CD133+ population) were chosen for functional evaluation of Ascl2 in colon cancer progenitor cells after gene knockdown by RNA interference. The microRNA (miRNA) microarrays identified 26 two-fold up-regulated miRNAs and 58 two-fold down-regulated miRNAs in shRNA-Ascl2/HT-29 cells and 178 two-fold up-regulated miRNAs and 172 two-fold down-regulated miRNAs in shRNA-Ascl2/LS174T cells. Two-condition experiment: shRNA-Ascl2/HT-29 cells vs. shRNA-Ctr/HT-29 cells, and shRNA-Ascl2/LS174T cells vs. shRNA-Ctr/LS174T cells. Biological replicates: 1 HT-29 cells stably transfected with shRNA-Ascl2/EGFP, 1 LS174T cells stably transfected with shRNA-Ascl2/EGFP, 1 HT-29 cells stably transfected with shRNA-Control/EGFP, and 1 LS174T cells stably transfected with shRNA-Control/EGFP, independently grown and harvested. One replicate per array.
Project description:CDK8 Mediator kinase is amplified and overexpressed in colon cancers; elevated CDK8 expression is associated with shorter patient survival. Nevertheless, CDK8 kinase inhibitors do not generally suppress colon cancer growth. We addressed this paradox by investigating the effects of CDK8 knockdown or a CDK8 kinase inhibitor on tumor growth at primary and metastatic sites. CDK8 knockdown or inhibition had no significant effect on primary tumors but suppressed the growth of hepatic metastases in murine and human colon cancer models. The effect of CDK8 inhibition on liver metastasis is mediated by upregulation of matrix metalloproteinase (MMP) inhibitor TIMP3 and downregulation of several MMPs.
Project description:CDK8 Mediator kinase is amplified and overexpressed in colon cancers; elevated CDK8 expression is associated with shorter patient survival. Nevertheless, CDK8 kinase inhibitors do not generally suppress colon cancer growth. We addressed this paradox by investigating the effects of CDK8 knockdown or a CDK8 kinase inhibitor on tumor growth at primary and metastatic sites. CDK8 knockdown or inhibition had no significant effect on primary tumors but suppressed the growth of hepatic metastases in murine and human colon cancer models. The effect of CDK8 inhibition on liver metastasis is mediated by upregulation of matrix metalloproteinase (MMP) inhibitor TIMP3 and downregulation of several MMPs.
Project description:Achaete scute-like 2 (Ascl2), a basic helix-loop-helix (bHLH) transcription factor, controls the fate of intestinal stem cells. However, the role of Ascl2 in colon cancer progenitor cells remains unknown. The cell lines HT-29 (47.5-95% of CD133+ population) and LS174T (0.45% of CD133+ population) were chosen for functional evaluation of Ascl2 in colon cancer progenitor cells after gene knockdown by RNA interference. The microRNA (miRNA) microarrays identified 26 two-fold up-regulated miRNAs and 58 two-fold down-regulated miRNAs in shRNA-Ascl2/HT-29 cells and 178 two-fold up-regulated miRNAs and 172 two-fold down-regulated miRNAs in shRNA-Ascl2/LS174T cells.
