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Enrichment of ornithine decarboxylase degron transduced colorectal cancer cells for extended application of cancer stem cell models [colorectal cancer]

ABSTRACT: Enrichment of ornithine decarboxylase degron transduced colorectal cancer cells for extended application of cancer stem cell models [colorectal cancer]

PROVIDER: PRJNA1186715 | ENA |

REPOSITORIES: ENA

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Enrichment of ornithine decarboxylase degron transduced colorectal cancer cells for extended application of cancer stem cell models [colorectal cancer]

Project description:Cancer stem cells (CSCs) are present in small quantities in tumor populations. To permit various analyses of CSCs, we attempted to enrich and expand ornithine decarboxylase (ODC) degron-transduced colorectal cancer (CRC) cells, which retain low proteasome activity. ZsGreen fluorescence-positive (ZsGreen+) cells were collected by sorting the ODC degron-transduced HCT116, DLD1, and SW480 cells, which were defined as enriched ZsGreen+ cells. ZsGreen+ cells still maintained CSC properties. These cells had higher stem cell marker expression and increased resistance to chemotherapy with 5-fluorouracil and oxaliplatin. ZsGreen+ HCT116 and DLD1 cells had greater sphere-forming ability and enhanced tumorigenicity compared to ZsGreen- control cells. Time-lapse microscopy showed that a single enriched ZsGreen+ HCT116 cell had asymmetric cell division. Thus, model CSCs were acquired in sufficient quantity. Using these cells, we performed a comprehensive microRNA analysis; miR- 491-3p was a candidate to suppress cancer stemness. Finally, we found that up- regulated genes in the enriched HCT116 ZsGreen+ cells correlated with those up- regulated in human clinical spheroid samples established from patient-derived xenografts derived from CRC tissue samples, further supporting the acquisition of enriched model CSCs. These cells would be useful in identifying novel CSC markers and developing medicine for anti-CSC therapy.

2025-07-09 | GSE282048 | GEO

Enrichment of ornithine decarboxylase degron transduced colorectal cancer cells for extended application of cancer stem cell models

Project description:Cancer stem cells (CSCs) are present in small quantities in tumor populations. To permit various analyses of CSCs, we attempted to enrich and expand ornithine decarboxylase (ODC) degron-transduced colorectal cancer (CRC) cells, which retain low proteasome activity. ZsGreen fluorescence-positive (ZsGreen+) cells were collected by sorting the ODC degron-transduced HCT116, DLD1, and SW480 cells, which were defined as enriched ZsGreen+ cells. ZsGreen+ cells still maintained CSC properties. These cells had higher stem cell marker expression and increased resistance to chemotherapy with 5-fluorouracil and oxaliplatin. ZsGreen+ HCT116 and DLD1 cells had greater sphere-forming ability and enhanced tumorigenicity compared to ZsGreen- control cells. Time-lapse microscopy showed that a single enriched ZsGreen+ HCT116 cell had asymmetric cell division. Thus, model CSCs were acquired in sufficient quantity. Using these cells, we performed a comprehensive microRNA analysis; miR-491-3p was a candidate to suppress cancer stemness. Finally, we found that up-regulated genes in the enriched HCT116 ZsGreen+ cells correlated with those up-regulated in human clinical spheroid samples established from patient-derived xenografts derived from CRC tissue samples, further supporting the acquisition of enriched model CSCs. These cells would be useful in identifying novel CSC markers and developing medicine for anti-CSC therapy.

2025-07-03 | GSE276573 | GEO

Enrichment of ornithine decarboxylase degron transduced colorectal cancer cells for extended application of cancer stem cell models

Project description:Enrichment of ornithine decarboxylase degron transduced colorectal cancer cells for extended application of cancer stem cell models

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Ornithine decarboxylase is sufficient for prostate tumorigenesis via androgen receptor signaling

Project description:Ornithine decarboxylase is sufficient for prostate tumorigenesis via androgen receptor signaling

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EPLIN-Beta is a novel substrate of ornithine decarboxylase antizyme 1, mediating cellular migration

Project description:Polyamines promote cellular proliferation, and their levels are controlled by ornithine decarboxylase antizyme 1 (Az1), through the proteasome-mediated, ubiquitin-independent degradation of ornithine decarboxylase (ODC), the rate-limiting enzyme of polyamine biosynthesis. Az1-mediated degradation of other substrates such as cyclin D1, DNp73 and Mps1 also regulate cell growth and centrosome amplification. Collectively, the currently known six Az1-substrates are all linked with tumorigenesis. To understand if Az1-mediated protein degradation might play a key role in regulating cellular process associated with tumorigenesis, we employed quantitative proteomics to identify novel Az1 substrates. Here, we describe the identification of LIM domain and Actin-binding protein 1 (LIMA1), also known as epithelial protein lost in neoplasm (EPLIN), as a new target of Az1. Interestingly, between the two isoforms of EPLIN-Alpha and -Beta, only EPLIN-Beta is the substrate of Az1, degraded in an ubiquitination-independent manner. Absence of Az1 led to elevated EPLIN-Beta levels, which caused enhanced cellular migration of Az1-/- cells. Consistently, higher levels of LIMA1 correlated with poorer overall survival of colorectal cancer patients. Taken together, this study identifies EPLIN-Beta as a novel Az1 substrate regulating cellular migration.

2023-06-08 | PXD039865 | Pride

Ornithine aminotransferase supports polyamine synthesis in pancreatic cancer

Project description:Pancreatic ductal adenocarcinoma (PDA) cells have a distinct dependence on de novo ornithine synthesis from glutamine via ornithine aminotransferase (OAT), which supports polyamine synthesis and is required for tumor growth. This directional OAT activity is normally largely restricted to infancy and contrasts with the reliance of most adult normal tissues and other cancer types on arginase (ARG) to generate arginine-derived ornithine, the substrate for polyamine synthesis. This dependence associates with arginine depletion in PDA tumor microenvironment, and is driven by mutant KRAS, which induces the expression of OAT and polyamine synthesis enzymes, including the rate-limiting enzyme ornithine decarboxylase-1 (ODC1). Loss of OAT, but not ARG2, largely mimics loss of ODC1, altering the transcriptional profiles in PDA cells, which in turn correlate with alterations in open chromatin states.

2023-01-01 | GSE193411 | GEO

Cancer-associated fibroblast-derived urea cycle metabolites promote colorectal cancer growth

Project description:Urea cycle (UC) dysfunction is linked to both tumorigenesis and poor prognosis in multiple cancers. However, the role of UC metabolism in tumor-stroma crosstalk is unclear. Here, we show that colorectal cancer (CRC) cells induce reprogramming of UC metabolism in cancer-associated fibroblasts (CAFs), which is mediated by CRC-derived exosomes. Reprogrammed CAFs support CRC cell growth by providing UC metabolites, especially arginine (Arg). Consequently, Arg deprivation resulted in growth inhibition of CRC cells. Furthermore, we found that Arg deprivation increases CRC’s dependence on putrescine (Put) and upregulates the expression of the polyamine biosynthetic rate-limiting enzyme ornithine decarboxylase (ODC). Combined Arg deprivation and ODC inhibitor effectively restrains CRC cell growth. Our study illustrates the UC metabolic interaction between CAFs and CRC cells and demonstrates the potential therapeutic utility of Arg restriction and ODC blockade combination treatment for colorectal cancer.

2025-01-31 | GSE285472 | GEO

Ornithine decarboxylase supports ILC3 responses in infectious and autoimmune colitis through positive regulation of IL-22 transcription

Project description:Group 3 innate lymphoid cells (ILC3s) are RORγT+ lymphocytes that are predominately enriched in mucosal tissues and produce IL-22 and IL-17A. They are the innate counterparts of Th17. While Th17 lymphocytes utilize unique metabolic pathways in their differentiation program, it is unknown whether ILC3s make similar metabolic adaptations. We employed single-cell RNA sequencing and metabolomic profiling of intestinal ILC subsets to identify an enrichment of polyamine biosynthesis in ILC3s, converging on the rate-limiting enzyme ornithine decarboxylase (ODC1). In vitro and in vivo studies demonstrated that exogenous supplementation with the polyamine putrescine or its biosynthetic substrate, ornithine, enhanced ILC3 production of IL-22. Conditional deletion of ODC1 in ILC3s impaired mouse antibacterial defense against C. rodentium infection, which was associated with a decrease in anti-microbial peptide production by the intestinal epithelium. Furthermore, in a model of anti-CD40 colitis, deficiency of ODC1 in ILC3s markedly reduced the production of IL-22 and severity of inflammatory colitis. We conclude that cell-intrinsic polyamine biosynthesis facilitates efficient defense against enteric pathogens as well as augments autoimmune colitis, thus representing an attractive target to modulate ILC3 function in intestinal disease.

2022-10-06 | GSE214152 | GEO

Ornithine Decarboxylase Activity in Gastric Epithelial Cells Contributes to the Pathogenesis of Helicobacter pylori

Project description:Ornithine Decarboxylase Activity in Gastric Epithelial Cells Contributes to the Pathogenesis of Helicobacter pylori

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Ornithine aminotransferase supports polyamine synthesis in pancreatic cancer

Project description:Ornithine aminotransferase supports polyamine synthesis in pancreatic cancer

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