GEO accession GSE215966 is currently private and is scheduled to be released on Aug 05, 2025.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA891354 | ENA |
REPOSITORIES: ENA
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Project description:Diverse taxa of fungus kingdom are part of cancer related microbiota but which fungi induce pro-tumor immune responses and whether they impact specific cancer pathways are unclear. Here, we use Cladosporium cladosporioides to orally infect mice lacking Ikka in epithelial stem cells. This infection promotes systemic inflammation, acidic oral milieu with Proteobacteria expansion, and oral and skin squamous cell carcinoma (SCC) development. Double Stat3 and Ikka deletions reverse these phenotypes. We found in the serum of mouse, C. cladosporioides induces IL-17a and Il-1b production. To investigate what is happening in the oral environment as well as in the skin cells of mice, we conducted 10x genomics single cell RNA sequencing on mRNA in oral buccal tissues and skins from Ikka inducible ablated mouse with fungi treatment (Cladosporium cladosporioides).
2026-08-20 | GSE215966 | GEO
Project description:Diverse taxa of fungus kingdom are part of cancer related microbiota but which fungi induce pro-tumor immune responses and whether they impact specific cancer pathways are unclear. Here, we use Cladosporium cladosporioides to orally infect wildtype mice or mice lacking Ikka or Stat3/Ikka in epithelial stem cells. This infection promotes systemic inflammation, acidic oral milieu with Proteobacteria expansion, and oral and skin squamous cell carcinoma (SCC) development. Double Stat3 and Ikka deletions reverse these phenotypes. We found in the serum of mouse, C. cladosporioides induces IL-17a and Il-1b production. To determine which cells contribute the upregulated level of Il-1b and Il17a in the blood under fungi treament, we conducted 10x genomics single cell RNA sequencing on mRNA in blood cells from WT, Ikka or Stat3/Ikka inducible ablated mice with fungi treatment (Cladosporium cladosporioides).
2026-08-20 | GSE223442 | GEO
Project description:scRNA seq of blood cells from Ikka or Stat3 inducible ablated mouse with fungi treatment
| PRJNA926327 | ENA
Project description:Depending on the tumor type IκB kinase α (IKKα) can act as tumor promoter or tumor suppressor in various malignancies. Here we demonstrate a key function of IKKα in the suppression of a tumoricidal microenvironment during intestinal carcinogenesis. Mice deficient in IKKα kinase activity are largely protected from intestinal tumor development that is dependent on the enhanced recruitment of IFNγ expressing M1-like myeloid cells. In IKKα mutant mice M1-like polarization is not controlled in a cell autonomous manner but depends rather on the interplay of both IKKα mutant tumor epithelia and immune cells. Tamoxifen-inducible β-catc.a. mice comprise an excellent model to study Wnt-dependent tumor initiation. These mice are characterized by IEC-restricted stabilization of β-catenin causing rapid expansion of intestinal crypts and loss of differentiated IEC. To further explore the underlying IKKα controlled pro-proliferative mechanism, we performed a microarray analysis comparing RNA isolated from wildtype, IkkαAA/AA, β-catc.a. or β-catc.a./IkkαAA/AA IEC 15 days after the first tamoxifen administration. and within 4 weeks β-catc.a. mice succumb to this marked crypt hyperproliferation
2014-06-01 | E-GEOD-51631 | biostudies-arrayexpress
Project description:Tumorigenicity of KRAS-ablated pancreatic cancer cells requires STAT3 function
| PRJNA1153379 | ENA
Project description:Depending on the tumor type IκB kinase α (IKKα) can act as tumor promoter or tumor suppressor in various malignancies. Here we demonstrate a key function of IKKα in the suppression of a tumoricidal microenvironment during intestinal carcinogenesis. Mice deficient in IKKα kinase activity are largely protected from intestinal tumor development that is dependent on the enhanced recruitment of IFNγ expressing M1-like myeloid cells. In IKKα mutant mice M1-like polarization is not controlled in a cell autonomous manner but depends rather on the interplay of both IKKα mutant tumor epithelia and immune cells.
2014-06-01 | GSE51631 | GEO
Project description:The skin exerts essential roles for the organism survival, such as environmental barrier and immune functions. IKKα is known as an essential protein for skin homeostasis. However, the functions performed by IKKα in the skin and the mechanisms it employs are largely unknown, leading to contradictory interpretations and results regarding the consequences of its deregulation in pathologies such as non-melanoma skin cancer (NMSC). Here, using our previously generated transgenic mouse models which express IKKα in the cytoplasm (C-IKKα mice) or in the nucleus (N-IKKα mice) of basal keratinocytes, we demonstrate that at each subcellular localization, IKKα distinctly regulates signaling pathways important for maintaining the balance between keratinocyte proliferation and differentiation, as well as the inflammatory response of the skin. As a result, N-IKKα mice show an atrophic epidermis with exacerbated terminal differentiation, reminiscent of alterations observed in patients with ichthyosis. Conversely, C-IKKα mice display a hyperplastic epidermis with impaired epidermal differentiation and pustular inflammation, resembling patients with pustular psoriasis. Interestingly, C-IKKα keratinocytes are almost devoid of nuclear IKKα due to endogenous IKKα downregulation. However, these changes in the skin of C-IKKα mice do not lead to the development of squamous cell carcinomas (SCCs), unlike N-IKKα mice, which develop spontaneous SCCs.
2024-11-14 | GSE239533 | GEO
Project description:Many patients have cancers that have increased activity of a protein called STAT3 that contributes critically to the development and growth of their cancer. Despite our knowledge of STAT3’s importance to cancer, scientists and doctors have not developed a drug that targets it and that patients can take to treat their cancer more effectively than treatments that are now available. Tvardi Therapeutics, Incorporated has developed a compound, TTI-101, which can be given by mouth and acts as a direct inhibitor of STAT3. Administration of TTI-101 to mice demonstrated that it blocked growth of cancers of the breast, head and neck, lung, and liver and it was safe when administered at high doses to mice, rats, and dogs. In this application, Tvardi is proposing to further develop TTI-101 for treatment of solid tumors for which the prognosis is dismal. The investigators will determine how safe it is when administered to patients with cancer, determine whether an adequate dose can be administered to patients with cancer that will block STAT3 in their cancer, and determine whether treatment with TTI-101 leads to reduced growth of their cancer.
| 2247646 | ecrin-mdr-crc
Project description:It has long been known that excessive mitotic activity due to H-Ras can block keratinocyte differentiation and cause skin cancer. It is not clear, however, whether there are any innate surveillants that ensure keratinocytes undergoing terminal differentiation, preventing the disease. IKKα induces keratinocyte terminal differentiation and its reduction promotes skin tumor development. However, its nature function in skin cancer is unknown. Here we found that mice with IKKα deletion in keratinocytes or in hair follicle keratinocytes developed a thickened epidermis and spontaneous squamous cell-like carcinomas. Inactivation of epidermal growth factor receptor (EGFR) or reintroduction of IKKα inhibited excessive mitosis, induced terminal differentiation, and prevented skin cancer through an EGFR-driven autocrine loop in mice. Thus, IKKα serves as an innate surveillant.
2009-07-14 | GSE12111 | GEO
Project description:Hepatitis C virus interacts extensively with host factors not only to establish productive infection but also to trigger unique pathological processes. Our recent genome-wide siRNA screen demonstrated that IKKα is a critical host factor for HCV. Here we describe a novel NF-κB-independent and kinase-mediated nuclear function of IKKα in HCV assembly. HCV infection, through its 3’-untranslated region, interacts with DDX3X to activate IKKα, which translocates to the nucleus and induces a CBP/p300-mediated transcriptional program involving SREBPs. This novel innate pathway induces lipogenic genes and enhances core-associated lipid droplet formation to facilitate viral assembly. Chemical inhibitors of IKKα suppress HCV infection and IKKα-induced lipogenesis, offering a proof-of-concept approach for novel HCV therapeutic development. Our results show that HCV commands a novel mechanism to its advantage by exploiting intrinsic innate response and hijacking lipid metabolism, which likely contributes to a high chronicity rate and the pathological hallmark of steatosis in HCV infection. Cells were treated with either non-targeting control siRNA or siRNA against IKKalpha. After 72 h, cells were either mock infected or infected with HCV JFH-1 strain with the M.O.I. of 0.5.
2013-05-08 | E-GEOD-46528 | biostudies-arrayexpress