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Through in vivo analyses, the study was intended to determine the effects of H89 on colon tumor formation and carcinogenesis. H89 delays colon cancer in BALB/c mice and chemically colon tumorigenesis, according to a preventive measure, and avoids tumor formation, which is reflected in an anti-tumor effect respectively. The antitumor effect of H89 was found to be linked to an increase in the tumor microenvironment of CD4+ T cells and CD8+ cytotoxic T cells, as well as a decrease in CD4+ Treg cells infiltration. In addition, qRT-PCR found that H89 can promote nave CD4+ T cell differentiation into Th1, reduces Treg differentiation, and boosts ex vivo CD8+ T cell-mediated cancer cell death of cancer cells. H89 promotes an overexpression of genes involved in antitumor immune response, such as IL-15RA, whose inhibition counteracts H89's antitumor immune response.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/811154
Patients in South Africa's indigenous African colorectal cancer patients are young, with no specific histopathological or molecular characteristics. According to their molecular subgroup status, RNA from FFPE tumour tissue from 3-4 CRC tumor samples was pooled according to their molecular subgroup status: 1 MSI-L LCC, 2 MSI-L RCC, 3 MSS LCC, and 4 MSS RCC were pooled; 1 MSI-L LCC, 2 MSI-L RCC, 3 MSS LCC, 4 MSS RCC, and 4 MSS RCC. Prior to gene expression analysis, the equal amount of total RNA from each sample was pooled before gene expression analysis.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/808962
Obesity is a worldwide epidemic linked to an elevated risk and colon cancer progression. When obese patients, local colon cancer patients had significant elevated ATGL levels in tumor tissue, which were significantly elevated relative to controls. Elevated ATGL levels in human colon cancer cells relative to non-transformed were boosted by an obesity mediator, oleic acid. Through retinoblastoma-mediated cell-cycle arrest, growth in CCC and colon cancer stem cells, which were rich in colon cancer stem cells, halted ATGL's degradation, stifled LDs utilization, and stifled OA-stimulated growth. Inhibition of ATGL in colonospheres has identified a target pathway in human colonic tumor crypt base cells isolated from colon cancer cells. These results show obesity-promoted, ATGL-mediated colonic tumor formation, as well as the determinant role of ATGL in obesity-related colon cancer progression. Overall plan: The investigation of ATGL-dependent transcription in colon cancer HT29 and HCT116 cells and their colonospheres.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/802850
Methods: In this research, a small dose of fluorouracil therapy against colon cancer cells had been used to simulate the situation in vivo when the cancer patients were receiving chemotherapy.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/798251
We had 27 adult patients who were scheduled to undergo elective colorectal cancer surgery between March and September, 2019. We performed metataxonomics analysis based on sequencing of the bacterial 16S rRNA gene marker, resulting in significant rises in the genus Enterococcus in both the preoperative and intraoperative samples and the post-operative sample, largely due to Enterococcus faecalis. Patients who received standard prophylaxis and carbapenems showed significant differences in the postoperative microbiome, especially in the family Erysipelotrichaceae.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/794543
5-Fluorouracil is one of the most common and widely used chemotherapeutic agents in colon cancer therapy. Dynamic reprogramming of chromatin accessibility allows for rapid access of the gene regulatory machinery to open genomic regions supporting subsequent gene expression by direct transcription factor activation and regulatory element binding. To better understand the regulatory network supporting 5-FU resistance in colon cancer cells, we investigated systematic variation of chromatin accessibility and transcript expression by the assay for transpose-accessible chromatin sequencing in tandem with transcriptome sequencing, followed by integrative analysis to identify potential regulators and their targets in 5-FU-resistant HCT15 cells. Based on findings about DEGs, DELs, and DEMs, a competitive endogenous RNAs regulatory network was created, indicating that H19, HOXA11-AS and NEAT1 may act as ceRNAs associated with 5-FU resistance in HCT15 cells. The TF DNA-binding motifs of FOX and KLF family members's were highly enriched in hyper- and hypo-accessible regions, respectively, as compared to AP-1 family and hypo-accessible areas. These findings provided clear insights and recommendations for an improved understanding of the non-genetic landscape of 5-FU-resistant colon cancer cells based on chromatin accessibility and transcript levels, which enabled for the detection of TF-binding sites, potential cis-regulatory elements, and therapeutic goals. In parental and 5-FU-resistant colon cancer cells, there has been a genome-wide analysis of chromatin availability and gene expression. HCM15-FR_1, mRNA+lncRNA-seq_HCT15-FR_1, mRNA+lncRNA_HCT15-FR_1, smRNA_HCT15-FR_1, smRNA-seq_HCT15-FR_1, smRNA_HCT15-FR_1, smRNA-seq_HCT15-FR_1, smRNA-seq_HCT15-FR_HCT15-FR_FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_HCT15-FR_1_FR_HCT15-FR_FR_FR_FR_1-FR_FR_FR_HCT15-FR_1.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/789176
We find that mouse and human colon cancer cells develop lymphocyte membrane proteins, including cellular markers such as CD4 and CD45. As a result of the transplant in vivo, cancer cells also obtained immune regulatory surface proteins like CTLA4 and Tim3, which inhibit immune cell activation. Compared to the non-trogocytic control, an ex vivo co-cultured splenocyte cell line with trogocytic cancer cells showed decreases in Th1 activation and natural killer cell signaling pathways. Cell trogocytosis was identified in patient-derived xenograft models of colorectal cancer and head and neck cancer.
Source link: https://www.ncbi.nlm.nih.gov/bioproject/775077
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