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P16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE213568 | GEO | 2023/08/02

REPOSITORIES: GEO

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p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer

Project description:We previously generated a mouse model of p16 epimutation (named as p16cis/cis) through targeted knock-in of a 140-bp Alu-related DNA sequence (cis-element) that facilitates the spread of DNA methylation at promoter CpG islands (CGIs) in cis (Yu et al. JCI, 2014). We generated primary mouse embryonic fibroblasts (MEFs) from p16cis/cis and control mice. By whole genome bisulfite sequencing (WGBS) for comprehensive DNA methylation profiling, we showed that cis-element-mediated approach specifically induces p16 promoter hypermethylation.

2023-08-02 | GSE214032 | GEO

p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer (scRNA-Seq)

Project description:Methylation of p16 promoter resulting in epigenetic gene silencing- known as p16 epimutation- is common in human colorectal cancer (CRC). Using mouse models, we demonstrated that p16 epimutation cooperates with mutant Apc to promote colon cancer development. To comprehensively characterize immune function within the tumor microenvironment (TME), we performed single-cell RNA sequencing (scRNA-seq) of colon tumors in these animals.

2023-08-02 | GSE213567 | GEO

p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer (RNA-Seq)

Project description:Using a mouse model of engineered p16 promoter hypermethylation (p16cis/cis), we found that p16 epimutation cooperates with mutant Apc to promote colon cancer development. Therefore, we performed RNA-seq analysis to identify genes regulated by p16 epimutation that contribute to intestinal carcinogenesis.

2023-08-02 | GSE213566 | GEO

p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer

Project description:p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer

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p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer

Project description:p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer

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p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer (RNA-Seq)

Project description:p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer (RNA-Seq)

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p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer (scRNA-Seq)

Project description:p16 epimutation modulates the tumor microenvironment and promotes malignancy of Apc-mutant colon cancer (scRNA-Seq)

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Recapitulating the human tumor microenvironment: Colon tumor-derived extracellular matrix promotes angiogenesis and tumor cell growth.

Project description:Extracellular matrix (ECM) is an essential and dynamic component of all tissues and directly affects cellular behavior by providing both mechanical and biochemical signaling cues. Changes in ECM can alter tissue homeostasis, potentially leading to promotion of cellular transformation and the generation of tumors. Therefore, understanding ECM compositional changes during cancer progression is vital to the development of targeted treatments. Previous efforts to reproduce the native 3D cellular microenvironment have utilized protein gels and scaffolds that incompletely recapitulate the complexity of native tissues. Here, we address this problem by extracting and comparing ECM from normal human colon and colon tumor that had metastasized to liver. We found differences in protein composition and stiffness, and observed significant differences in vascular network formation and tumor growth in each of the reconstituted matrices, both in vitro and in vivo. We studied free/bound ratios of NADH in the tumor and endothelial cells using Fluorescence Lifetime Imaging Microscopy as a surrogate for the metabolic state of the cells. We observed that cells seeded in tumor ECM had higher relative levels of free NADH, consistent with a higher glycolytic rate, than those seeded in normal ECM. These results demonstrate that the ECM plays an important role in the growth of cancer cells and their associated vasculature.

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Midostaurin Modulates Tumor Microenvironment and Enhances Efficacy of Anti-PD-1 against Colon Cancer.

Project description:Immunotherapy modulating the tumor microenvironment (TME) immune function has a promising effect on various types of cancers, but it remains as a limited efficacy in colon cancer. Midostaurin (PKC412) has been used in the clinical treatment of fms-like tyrosine kinase 3 (FLT3)-mutant acute myeloid leukemia and has demonstrated immunomodulatory activity. We aimed to evaluate the effect of midostaurin on the modulation of TME and the efficacy of anti-programmed cell death protein 1 (PD-1) against colon cancer. Midostaurin inhibited the growth of murine CT26 and human HCT116 and SW480 cells with multinucleation and micronuclei formation in morphology examination. The cell cycle arrested in the G2/M phase and the formation of the polyploid phase was noted. The formation of cytosolic DNA, including double-strand and single-strand DNA, was increased. Midostaurin increased mRNA expressions of cGAS, IRF3, and IFNAR1 in colorectal adenocarcinoma cells and mouse spleen macrophages. The protein expressions of Trex-1, c-KIT, and Flt3, but not PKCα/β/γ and VEGFR1, were down-regulated in midostaurin-treated colorectal adenocarcinoma cells and macrophages. Trex-1 protein expression was abrogated after FLT3L activation. In vivo, the combination of midostaurin and anti-PD-1 exhibited the greatest growth inhibition on a CT26-implanted tumor without major toxicity. TME analysis demonstrated that midostaurin alone decreased Treg cells and increased neutrophils and inflammatory monocytes. NKG2D+ and PD-1 were suppressed and M1 macrophage was increased after combination therapy. When combined with anti-PD-1, STING and INFβ protein expression was elevated in the tumor. The oral administration of midostaurin may have the potential to enhance anti-PD-1 efficacy, accompanied by the modulation of cytosolic DNA-sensing signaling and tumor microenvironment.

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CHPF promotes malignancy of breast cancer cells by modifying syndecan-4 and the tumor microenvironment.

Project description:Breast cancer is the leading cause of cancer-related deaths in women worldwide. Several studies have indicated that abnormal chondroitin sulfate (CS) chains accumulate in breast cancer tissues; however, the functions and dysregulation of CS synthases are largely unknown. Here, we demonstrate that chondroitin polymerising factor (CHPF) is frequently upregulated in breast cancer tissues and that its high expression is positively associated with tumor metastasis, high stages, and short survival time. CHPF modulates CS formation in breast cancer cells. Additionally, we found that CHPF promotes tumor growth and metastasis accompanied by an increase in G-CSF levels and the number of myeloid-derived suppressor cells in tumor tissue. We revealed that tumor cell-derived G-CSF is co-localised with CS on the cell surface. Interestingly, our study is the first to identify that syndecan-4 (SDC4) is modified by CHPF and that it is involved in CHPF-mediated phenotypes. Moreover, breast cancer patients with high expression of both SDC4 and CHPF had worse overall survival compared to other subsets, which implied the synergistic effects of these two genes. In summary, our results indicated that the upregulation of CHPF in breast cancer contributes to the malignant behaviour of cancer cells, thereby providing novel insights on the significance of CHPF-modified SDC4 in breast cancer pathogenesis.

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