Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1160906 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The transcriptional repressor Capicua (CIC) is negatively regulated by KRAS/MAPK signaling. To characterize the impact of CIC loss on KrasG12V/Trp53-KO-driven lung adenocarcinomas in mice, the transcriptome of tumors from Kras (+/LSLG12V); Trp53 (lox/lox) [KP] and Kras (+/LSLG12V); Trp53 (lox/lox); Cic (lox/lox) [KPCic] mice are compared.
2025-09-11 | GSE303269 | GEO
Project description:CIC binding was determined in KP murine lung cancer cells in untreated cells as well as after treatment with trametinib to enhance CIC binding to DNA. As a negative control, CIC binding was also determined in KPCic cells that express a non-functional CIC incapable of DNA binding.
2025-09-11 | GSE303110 | GEO
Project description:Ubiquitin-specific peptidase 22 (USP22), a deubiquitinase and component of the “Death-By-Cancer” 11-gene signature, is overexpressed in multiple cancers and linked to recurrence, therapy resistance, and poor prognosis. While its role in tumor immune evasion is emerging, the function of USP22 in KRAS-driven lung cancer and antitumor immunity remains largely unknown. Given that oncogenic KRAS promotes an immunosuppressive tumor microenvironment (TME) and resistance to immunotherapy, this study investigates USP22's role in KRAS-driven lung cancer and its potential impacts on carcinogenesis and anticancer immunity. For this purpose, Usp22 knockout (Usp22-KO) mouse model was developed in the KRASG12D; p53−/− (KP) background, cancers were induced, and spatial transcriptomics was applied to define the difference in TME of mouse KP verse USP22-KO-KP (KPU-) lung cancer.
2026-08-20 | GSE306019 | GEO
Project description:Ubiquitin-specific peptidase 22 (USP22), a deubiquitinase and component of the “Death-By-Cancer” 11-gene signature, is overexpressed in multiple cancers and linked to recurrence, therapy resistance, and poor prognosis. While its role in tumor immune evasion is emerging, the function of USP22 in KRAS-driven lung cancer and antitumor immunity remains largely unknown. Given that oncogenic KRAS promotes an immunosuppressive tumor microenvironment (TME) and resistance to immunotherapy, this study investigates USP22's role in KRAS-driven lung cancer and its potential impacts on carcinogenesis and anticancer immunity. For this purpose, Usp22 knockout (Usp22-KO) mouse model was developed in the KRASG12D; p53−/− (KP) background, cancers were induced, and bulk RNA-seq analysis was applied to indentify differentially expressed genes and alterated signaling pathways in USP22-KO-KP (KPU-) lung cancers, compared to KP lung cancers.
2026-08-20 | GSE306017 | GEO
Project description:Polycomb repressive complexes (PRC) are frequently implicated in human cancer acting either as oncogenes or tumor suppressors. Here we show that PRC2 is a critical regulator of Kras-driven non-small-cell lung cancer (NSCLC) progression. Modulation of PRC2 by either Ezh2 overexpression or Eed deletion enhances Kras-driven adenomagenesis and inflammation, respectively. Eed-loss-driven inflammation leads to massive macrophage recruitment and marked decline in tissue function. Additional Trp53 inactivation activates a cell autonomous epithelial-to-mesenchymal transition (EMT) program leading to an invasive mucinous adenocarcinoma. A switch between methylated/acetylated chromatin underlies the tumor phenotypic evolution, prominently involving genes controlled by Hippo/Wnt-signaling. Our observations in the mouse models were conserved in human cells. Importantly, PRC2 inactivation results in context-dependent phenotypic alterations, with implications for its therapeutic application. We generated ChIP-seq from primary Kras;p53 (KP) cells in culture with and without Eed (KPE) and from KP primary tumors generated by injection of NSCLC into the tail vein. Mice were sacrificed on the onset of shortness of breath. We generated genome-wide expression profiles (RNA-seq) and Nuclease Accessibility (NA)-seq in primary KP and KPE tumor cells. NA-seq was also performed in A549 cells.
2016-01-15 | E-GEOD-61190 | biostudies-arrayexpress
Project description:We performed single-cell RNA sequencing (scRNAseq) analysis on the mouse lung tissues from KP tumor-bearing mice treated with tumor cell intrinsic Asf1a KO, anti-PD-1 or combination treatment
2019-11-26 | GSE133604 | GEO
Project description:Here, we using CRISPR activation and knockout studies to assess the implication of dysregulation of RUNX transcription factors on chromatin accessibility using bulk ATAC-sequencing. Tumor cell lines were derived from primary Kras G12D; p53 mutant mice (KP model) after initiation of tumors with SPC-Cre, resulting in lung adenocarcinoma. Cell lines were then expanded and profiled using bulk ATAC-sequencing.
2020-07-23 | GSE151403 | GEO
Project description:To investigate the chemokines expressed by the KP cancer line and to compare it to chemokines expressed in lung tissues upon inoculation of KP tumor cells
2022-04-07 | GSE200126 | GEO
Project description:Despite substantial progress in lung cancer immunotherapy, the overall response rate in KRAS-mutant lung adenocarcinoma (ADC) patients remains low. Combining standard immunotherapy with adjuvant approaches that enhance adaptive immune responses—such as epigenetic modulation of anti-tumor immunity—is therefore an attractive strategy. To identify epigenetic regulators of tumor immunity, we constructed an epigenetic-focused sgRNA library, and performed an in vivo CRISPR screen in KrasG12D/P53-/- (KP) lung ADC model. Our data showed that loss of the histone chaperone Asf1a in tumor cells sensitizes tumors to anti-PD-1 treatment. Mechanistic studies revealed that tumor cell intrinsic Asf1a deficiency induced immunogenic macrophage differentiation in the tumor microenvironment by upregulating GM-CSF expression and potentiated T cell activation in combination with anti-PD-1. Our results provide a rationale for a novel combination therapy consisting of Asf1a inhibition and anti-PD-1 immunotherapy.
2019-11-26 | GSE138571 | GEO