Project description:This dataset contains raw ChIP-seq data from esophageal squamous cell carcinoma (ESCC) cells overexpressing TFAP2β or its LLPS-deficient mutants (ΔIDR3 or Mut_IDR3). The experiment aims to explore the chromatin binding profiles of TFAP2β and its phase separation-deficient mutants to uncover the role of TFAP2β's LLPS activity in regulating gene expression in ESCC. Data were collected from the genomic binding of TFAP2β and its LLPS-deficient mutants, providing insights into the regulatory networks controlled by TFAP2β in cancer progression.
Project description:To explore the role of smooth muscle cell (SMC) Ano1 in atherosclerosis, Ano1 SMC-sepcific knockout mice (Ano1<SMCKO>) and the control mice (WT<SMC>) were injected with AAV-PCSK9DY followed by feeding a high-fat diet for 12 weeks. Subsequently, mouse aortic SMCs (MASMCs) were isolated and subjected to Chip sequencing (ChIP-seq) analysis.
Project description:This dataset contains raw RNA-seq data from esophageal squamous cell carcinoma (ESCC) cells overexpressing GFP-TFAP2β, its LLPS-deficient mutants (ΔIDR3 and Mut_IDR3) or GFP control. The experiment aims to explore the downstream genes of TFAP2β and its phase separation-deficient mutants to uncover the role of TFAP2β's LLPS activity in regulating gene expression in ESCC. Data were collected from the genomic binding of TFAP2β and its LLPS-deficient mutants, providing insights into the regulatory networks controlled by TFAP2β in cancer progression.
Project description:The calcium-activated chloride channel ANO1 (TMEM16A) is overexpressed in colorectal cancer (CRC) and associated with poor prognosis, but its role in regulating metastatic plasticity is not fully understood. To elucidate the transcriptomic networks governed by ANO1, we performed RNA sequencing on SW620 CRC cells stably expressing sh-control or sh-ANO1. Total RNA was extracted using Trizol reagent. Sequencing libraries were constructed with the NEBNext® Ultra RNA Library Prep Kit for Illumina® and sequenced on an Illumina Novaseq platform, generating 125-150 bp paired-end reads. Bioinformatics analysis included read alignment with HISAT2 (v2.0.5) and differential expression analysis using DESeq2 (v1.20.0) with a threshold of |log2(Fold Change)| ≥ 1 and adjusted p-value < 0.05. Functional enrichment analysis for Gene Ontology (GO) and KEGG pathways was performed with clusterProfiler (v3.8.1). Gene Set Enrichment Analysis (GSEA) was conducted using gene sets from MSigDB. Transcriptomic profiling identified 1,894 differentially expressed genes (DEGs) upon ANO1 knockdown, with 1,523 downregulated and 371 upregulated. Downregulated genes included key EMT and signaling components (e.g., PIK3C2A, PIK3CA, KRAS, ZEB1). GO analysis revealed enrichment in processes related to genomic integrity and cell division. KEGG pathway analysis highlighted significant enrichment in “Homologous recombination” and “Platinum drug resistance”. A trend-level downregulation was observed for the “mTOR signaling pathway”. This dataset illustrates that ANO1 knockdown drives broad changes in a pro-metastatic transcriptome network and implicates mTOR signaling as a potential downstream mechanism, providing a resource for understanding how ANO1 promotes CRC progression.
Project description:The overall goal of this study was to compare gene expression profiles in MOAB-overexpressing PrSC cells and control cells, also to compare gene expression profiles in MAOB-knockdown and control cells.
