colorectal carcinoma cell line ht 29  (Procell Inc)

Journal: Frontiers in Genetics

Article Title: Integrated promoter-capture Hi-C and Hi-C analysis reveals fine-tuned regulation of the 3D chromatin architecture in colorectal cancer

doi: 10.3389/fgene.2025.1553469

Figure Lengend Snippet: Schematic diagram of the workflow for the identification of target genes. Graphical representation of the steps used in the analysis combining multiple large colorectal cancer datasets (PCHi-C, Hi-C, ChIP-seq, RNA-seq, and single-cell RNA-seq) to identify target genes potentially playing a key role in CRC progression.

Article Snippet: HT29 colorectal carcinoma cell line (ATCC, HTB-38) was cultured in DMEM, with 10% FBS and antibiotics.

Techniques: Hi-C, ChIP-sequencing, RNA Sequencing

Journal: Frontiers in Genetics

Article Title: Integrated promoter-capture Hi-C and Hi-C analysis reveals fine-tuned regulation of the 3D chromatin architecture in colorectal cancer

doi: 10.3389/fgene.2025.1553469

Figure Lengend Snippet: Comparison of the distribution of TADs and genes within TADs between case cell lines (HT29 and LoVo) and control cell lines (hESC and FHC). Here, TAD refers to intra-chromosomal interaction between two different genomic fragments. (A) Number of TAD boundaries against hESC, FHC, HT29, and LoVo cell lines generated by HiCExplorer. (B) Number of genes located within disrupted TADs in control (hESC and FHC) versus case (HT29 and LoVo) cell lines. (C) Venn diagram depicting genes within disrupted TADs between control and case groups.

Article Snippet: HT29 colorectal carcinoma cell line (ATCC, HTB-38) was cultured in DMEM, with 10% FBS and antibiotics.

Techniques: Comparison, Control, Generated

Journal: Frontiers in Genetics

Article Title: Integrated promoter-capture Hi-C and Hi-C analysis reveals fine-tuned regulation of the 3D chromatin architecture in colorectal cancer

doi: 10.3389/fgene.2025.1553469

Figure Lengend Snippet: Distribution of promoter-capture Hi-C interactions in hESC, HT29, and LoVo cell lines. Here, bait fragment refers to the promoter-capture region or region of interest and other-end fragment refers to those fragments that interact with the bait fragment. (A) Proportion of bait interactions with other ends generated by CHiCAGO using PCHiC data of HESC, HT29, and LoVo cell lines. (B) Venn diagram displaying the number of bait fragments among hESC, HT29, and LoVo. (C) Interaction counts of bait fragments with other-end fragments of hESC, HT29, and LoVo cell lines. (D) Chromosome-wise interaction counts of bait fragments with other-end fragments of hESC, HT29, and LoVo cell lines. The black curve depicts chromosome lengths as per the reference genome GRCh38.

Article Snippet: HT29 colorectal carcinoma cell line (ATCC, HTB-38) was cultured in DMEM, with 10% FBS and antibiotics.

Techniques: Hi-C, Generated

Journal: Frontiers in Genetics

Article Title: Integrated promoter-capture Hi-C and Hi-C analysis reveals fine-tuned regulation of the 3D chromatin architecture in colorectal cancer

doi: 10.3389/fgene.2025.1553469

Figure Lengend Snippet: Distribution of differential promoter-capture Hi-C interactions between cancer cell lines (HT29 and LoVo) versus normal cell line (hESC). (A) Pie-chart depicting proportions of differential bait interactions between cancer versus normal cell lines. (B, C) Differential bait interaction counts of cancer versus normal cell lines with respect to bait fragments. (D, E) Differential interaction detected by Chicdiff around HDAC1, MARCKSL1, and SMARCC1 genes are plotted. Significant interactions were detected for each condition separately by CHiCAGO and color-coded (blue: 3 < score ≤ 5; red: score >5). Significant differentially interacting regions detected by Chicdiff were depicted as red blocks against HT29 versus hESC and LoVo versus hESC cell lines. (F) Volcano plot of differentially expressed genes generated from the colorectal cancer dataset from TCGA database. A total of 57,864 transcripts were observed. A total of 27,676 statistically significant transcripts were identified (false discovery rate ≤ 0.05), out of which 17,146 transcripts were expressed in cancer cells, while 10,530 transcripts were expressed in normal cells.

Article Snippet: HT29 colorectal carcinoma cell line (ATCC, HTB-38) was cultured in DMEM, with 10% FBS and antibiotics.

Techniques: Hi-C, Generated

Journal: Frontiers in Genetics

Article Title: Integrated promoter-capture Hi-C and Hi-C analysis reveals fine-tuned regulation of the 3D chromatin architecture in colorectal cancer

doi: 10.3389/fgene.2025.1553469

Figure Lengend Snippet: Distribution of genome-wide interactions between CRC cell lines (HT29 and LoVo) and embryonic stem cell line (hESC). Here, TAD refers to intra-chromosomal interaction between two different genomic fragments. (A) Number of TAD boundaries for each cell line generated by HiCExplorer ( ; ; ). (B) Number of conserved and disrupted TADs between the two cell lines. (C) TAD plot of chr1:28788062–35788062 of HT29, hESC, and LoVo cell lines, and red rectangle highlights a major TAD shift of HT29 and LoVo compared to hESCs. (D) Affected genes due to shifting of TAD boundaries in HT29 and LoVo cell lines compared with hESCs. (E) Numbers of protein-coding and non-coding genes in HT29 and LoVo TADs compared with those in hESC TADs.

Article Snippet: HT29 colorectal carcinoma cell line (ATCC, HTB-38) was cultured in DMEM, with 10% FBS and antibiotics.

Techniques: Genome Wide, Generated

Journal: Frontiers in Genetics

Article Title: Integrated promoter-capture Hi-C and Hi-C analysis reveals fine-tuned regulation of the 3D chromatin architecture in colorectal cancer

doi: 10.3389/fgene.2025.1553469

Figure Lengend Snippet: Functional annotation of genes extracted from TAD disruption regions and proportion of cis-regulatory interaction with bait fragments. (A) Network visualization of genes and gene families associated with chromatin remodeling (green), chromatin assembly (blue), and chromatin organization (red). (B) Volcano plot showing the expression pattern of chromatin remodeling, chromatin assembly, and chromatin organization associated genes that had been extracted from Gene Ontology analysis. (C) Total number of bait interactions with regulatory elements (promoter-like (PLS), proximal enhancer-like (pELS), distal enhancer-like (dELS), DNase-H3K4me3, and CTCF regions in disrupted TAD regions of hESC and HT29 cell lines in hESC/HT29. (D) Total number of bait interactions with regulatory elements (promoter-like (PLS), proximal enhancer-like (pELS), distal enhancer-like (dELS), DNase-H3K4me3, and CTCF regions in disrupted TAD regions of hESC and LoVo cell lines in hESC/LoVo.

Article Snippet: HT29 colorectal carcinoma cell line (ATCC, HTB-38) was cultured in DMEM, with 10% FBS and antibiotics.

Techniques: Functional Assay, Disruption, Expressing

Journal: Frontiers in Genetics

Article Title: Integrated promoter-capture Hi-C and Hi-C analysis reveals fine-tuned regulation of the 3D chromatin architecture in colorectal cancer

doi: 10.3389/fgene.2025.1553469

Figure Lengend Snippet: Impact of structural changes on gene regulation between cancer cell lines (HT29 and LoVo) and normal cell lines (hESCs). (A) The ∼ 7 Mb region of chromosome 18 encompassing the DSG4 gene is shown along with TAD boundaries of Hi-C interaction maps at 10 Kb resolution for case (HT29 and LoVo) and control (hESC). (B) Zoomed-in view of the DSG4 locus in case (HT29 and LoVo) and control (hESC) along with corresponding PCHi-C interactions and ChIP-seq data for H3K27ac and H3K4me1 are displayed in blue peaks. Filtered DSG4 read counts used by CHiCAGO are displayed in red, with the corresponding significant interactions shown as arcs. For clarity, only DSG4 interactions were shown.

Article Snippet: HT29 colorectal carcinoma cell line (ATCC, HTB-38) was cultured in DMEM, with 10% FBS and antibiotics.

Techniques: Hi-C, Control, ChIP-sequencing

Journal: Frontiers in Genetics

Article Title: Integrated promoter-capture Hi-C and Hi-C analysis reveals fine-tuned regulation of the 3D chromatin architecture in colorectal cancer

doi: 10.3389/fgene.2025.1553469

Figure Lengend Snippet: Validation of target genes extracted from integrative analysis. (A) qRT-PCR analysis of target genes in NT2D1, HT29, Colo205, HCT15, and DLD1 cell lines, showing relative enrichment of gene expression in the CRC cell lines compared to NT2D1 cells. (B, C) ChIP-qPCR for H3K4me3 and H3K27ac modifications, respectively, on the transcription start site (TSS) upstream regions of target genes. The cell lines used are indicated below the bars. Three biological replicates were used for statistical analysis using GraphPad v9.1. A one-way ANOVA or unpaired t-test was used as the significance test. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, and ns,non-significant.

Article Snippet: HT29 colorectal carcinoma cell line (ATCC, HTB-38) was cultured in DMEM, with 10% FBS and antibiotics.

Techniques: Biomarker Discovery, Quantitative RT-PCR, Gene Expression, ChIP-qPCR

Journal: Frontiers in Genetics

Article Title: Integrated promoter-capture Hi-C and Hi-C analysis reveals fine-tuned regulation of the 3D chromatin architecture in colorectal cancer

doi: 10.3389/fgene.2025.1553469

Figure Lengend Snippet: Schematic depiction of the architectural changes in TADs during tumorigenesis: we explored how dynamic changes in the 3D genome architecture influence gene regulation in colorectal cancer (CRC). Fine-scale 3D-genome interactions, combined with their association with epigenomic marks, were analyzed to identify novel biomarkers for CRC progression. The disruption of TAD dynamics was found to involve a subset of colorectal-specific genes, as depicted schematically.

Article Snippet: HT29 colorectal carcinoma cell line (ATCC, HTB-38) was cultured in DMEM, with 10% FBS and antibiotics.

Techniques: Disruption